London · New York · Monaco
Peptide Clinic
London
Peptide Therapy
Diagnostics-First.
100% personalized to you — always. A doctor-guided approach built on your individual analysis and comprehensive blood tests.
The Catalyst Clinic is a doctor-led peptide clinic in London, with consultations also in New York, Monaco and remotely. Every peptide therapy consultation is personally overseen by Dr. Ethan Hausman-Marquis — a doctor-scientist with a PhD in Cell and Genomic Biology, nearly 20 years of specialist peptide research experience, and three published books in this field. Every consultation begins with mandatory comprehensive bloodwork, and we offer optional comprehensive genetic and genomic testing for patients who want DNA-level preventive precision. No advisory program is discussed without your data.
Consultation Overview
Initial Consultation
60 minsIn-person or remote
Diagnostics Required
Yes — Included in LondonMandatory before every advisory consultation · included in the fee in London
DEXA Body Scan
Included in LondonObjective tracking of fat, lean muscle and bone density · included in the monthly fee in London
Monthly Reviews
IncludedPersonal oversight from your doctor throughout
Repeat Diagnostics
Every 4–5 monthsProgram evolves with your data
Source Standards
GMP-CertifiedEMA-regulated · FDA-registered· US and European-prescription peptides
Doctor's Credentials
PhD-LevelThe only published peptide doctor-scientist in Europe
Genetic & Genomic Testing
Optional Add-OnDNA-level precision · feeds AURION™ · counseling included
Program Price
From £600/monthInitial consultation £200 · Diagnostics and DEXA included in London · Remote available worldwide
All compounds prescribed exclusively from GMP-certified, EMA-regulated and FDA-registered compounding pharmacies. Certificate of analysis on every order. Not licensed medicines under the Human Medicines Regulations 2012. Genetic testing is optional and provided as accredited clinical diagnostic testing.
The Science
What Is Peptide Therapy?
Peptides are short chains of amino acids — the fundamental building blocks of proteins. They occur naturally throughout the human body, where they act as signaling molecules, instructing cells to carry out specific biological functions.
Because peptides are involved in a vast range of physiological processes — from tissue repair and metabolic regulation to neurological signaling and immune modulation — they represent one of the most active and promising areas of contemporary biological research.
In clinical practice, peptide therapy means a doctor prescribing specific peptides after assessment, most often as small subcutaneous injections given with a pen device, and monitoring the response with repeat bloodwork. That monitoring is the difference between a peptide clinic and buying peptides online.
At our London peptide clinic, advisory consultations are grounded in the current scientific literature surrounding these compounds. Dr. Ethan Hausman-Marquis has spent nearly two decades researching peptide biology and has published three books in the field.
It is important to understand that the compounds discussed are research compounds. They are not licensed medicines, and our role is advisory — helping scientifically curious patients understand the research in the context of their own biomarker data.
Key Characteristics
- Short chains of amino acids (typically 2–50)
- Naturally occurring signaling molecules
- Highly specific biological interactions
- Active area of regenerative research
- Studied across multiple physiological systems
- Not licensed medicines under UK regulations
Advisory Programs Tailored To Your Biology
Peptide Therapy Programs
The Catalyst Method is built entirely around your biomarker data and current scientific literature. The following areas represent the primary themes of peptide compound research that Dr. Ethan consults on at our London peptide clinic and remotely. Every program is 100% personalized to you — always. No two patients receive the same advisory protocol, because no two patients have the same biology. Optional genetic and genomic testing can add a further, DNA-level layer of preventive precision to any program.
Performance & Recovery
An area of active scientific investigation exploring how certain peptide compounds may interact with musculoskeletal and recovery-related biological pathways. Research in this area examines compounds for their potential roles in tissue biology and recovery-related cellular processes.
- Tissue repair biology research
- Musculoskeletal pathway investigation
- Inflammatory modulation research
- Recovery-related biological pathways
Cognitive & Mood
An emerging field of research examining how certain neuropeptide compounds may interact with neurological and mood-related biological systems. Research in this area examines compounds for their potential interactions with neurotrophic and neurological signaling pathways.
- Neuropeptide research
- Neurological signaling investigation
- Neuroplasticity research
- Mood-related biological systems
Longevity & Metabolic
A growing area of scientific inquiry into how certain peptide compounds may interact with metabolic and longevity-related biological pathways. Research examines compounds for their potential interactions with metabolic, mitochondrial, and biological aging pathways.
- Biological aging research
- Metabolic pathway investigation
- Mitochondrial biology research
- Longevity-related pathway research
Peptides Explained
Peptides in Two Minutes
An animated introduction to how these small protein molecules are being studied for their roles in cell biology, signaling, and regenerative research.
Follow peptides through their proposed biological interactions — created by Dr. Ethan Hausman-Marquis
The Podcast
The Science of Ageless Living
The UK's Leading Peptide Research Podcast
Hosted by Dr. Ethan Hausman-Marquis — doctor-scientist with a PhD in Cell and Genomic Biology and one of the world's leading peptide researchers. The Science of Ageless Living is a leading podcast dedicated to peptide research, longevity science, and biological optimization — designed to give listeners the scientific context they need to make genuinely informed decisions about their health.
Every episode is grounded in peer-reviewed research. No commercial agenda. No supplements to sell. Just the science — explained by the only doctor in London who has spent nearly 20 years researching it and published three books in the field. If you are considering a consultation at The Catalyst Clinic, we actively encourage you to listen first. An informed patient is always a better-served patient.
Your Journey
Your 6-Step Catalyst Method
Our approach is built on one principle: responsible advisory consultations involving peptide compounds require diagnostics before everything, a doctor who reads your results personally, and clinical oversight that continues for as long as you are with us.
Step 01
Blood, Physiological & Genetic Testing
Every program begins with a full blood panel. This is included in the price in London. No advisory consultation is conducted without your data. This is the foundation of everything that follows — without it, no responsible advisory program can be designed. As an empirical way of measuring success in body composition, we perform DEXA body scans. Optional comprehensive preventive DNA testing can be added to build a lifelong genetic baseline alongside your bloodwork.
- Complete Blood Count (CBC)
- Comprehensive Metabolic Panel
- Full hormone panel including sex hormones
- Inflammatory markers
- DEXA body scanning
- Comprehensive preventive DNA testing (optional)
- Additional biomarkers relevant to your goals
Step 02
Biomarker-Guided Selection
Dr. Ethan reviews your results personally — not via algorithm, not via delegation. He identifies which areas of peptide compound research are relevant to your specific biomarker profile, health history, and goals.
- Goal-specific compound research matching
- Health profile analysis
- Biomarker-guided selection
- Safety and contraindication screening
Step 03
Bespoke Advisory Protocol
A fully personalized prescribed peptide advisory program designed around your data. No two protocols at The Catalyst Clinic are identical. Every recommendation is documented, explained, and traceable.
- Compounded personalized prescribed research selection
- Dosage rationale and guidance
- Delivery method guidance
- Complete transparency throughout
Step 04
Induction & Ongoing Reviews
A structured induction session ensures you understand every element of your advisory program. Monthly doctor reviews are included as standard. Bloodwork is repeated every four to five months.
- Detailed induction session
- Monthly progress reviews
- Program adjustments based on data
- Repeat bloodwork every 4–5 months
Step 05
Strategic Cycling
Advisory programs at The Catalyst Clinic are designed with cyclicity — preventing biological adaptation, maintaining natural hormonal homeostasis, and optimizing long-term outcomes.
- Prevents biological adaptation
- Maintains natural homeostasis
- Avoids endocrine complications
- Optimizes long-term program design
Step 06
Full Transparency
Every decision is documented, explained, and traceable. You will receive full written documentation of your advisory program and the scientific rationale behind every recommendation.
- Full medical history discussion
- Medication interaction screening
- Open communication channels throughout
- Educational approach at every stage
Research Compounds — Scientific Reference
Top Peptides — Full Biochemistry
A complete scientific reference for each compound — amino acid sequences, molecular weight, receptor targets, signaling pathways, gene interactions, and mechanism of action. Written for doctors, researchers, and scientifically literate patients who want to understand the biochemistry behind the research.
01 · BPC-157 Performance & Recovery
Body Protection Compound 157
- Molecular weight
- 1,419.53 Da
- Length
- 15 amino acids
- Formula
- C₆₂H₉₈N₁₆O₂₂
- Half-life
- ~4 hours (subcutaneous)
- Origin
- Gastric juice protein fragment
Overview
BPC-157 is a synthetic pentadecapeptide derived from the body protection compound found in human gastric juice. It is gastric acid-stable, which distinguishes it from most endogenous peptides. The sequence is derived from a 44-amino acid gastric peptide (BPC) identified in human gastric juice in the 1990s.
Mechanism of action — under investigation
BPC-157 research centers on its interactions with the nitric oxide (NO) system. Studies suggest it may upregulate eNOS (endothelial nitric oxide synthase) and modulate NO production, promoting vasodilation and angiogenesis. It also appears to interact with the FAK-paxillin pathway involved in cell migration and cytoskeletal organization, and may modulate VEGF (vascular endothelial growth factor) expression.
Signaling pathways under investigation
- NO/eNOS Pathway: Proposed upregulation of eNOS; increased NO production studied in endothelial cells — may drive vasodilation and angiogenesis
- FAK-Paxillin: Interactions with focal adhesion kinase and paxillin studied; may modulate cell migration and wound healing
- VEGF Signaling: Modulation of VEGF expression studied in preclinical models; proposed role in angiogenesis and tissue repair
- Dopamine System: Preclinical studies suggest modulation of dopamine D1 and D2 receptor activity and dopamine turnover
- Serotonin System: Studies suggest interactions with 5-HT synthesis and receptor activity in CNS models
- Cytoskeletal Organization: Interactions with actin polymerization and cytoskeletal dynamics studied in cell migration research
Receptor interactions
No single high-affinity receptor identified to date. Research suggests promiscuous binding interactions with growth factor receptors and NO system components. FAK and paxillin interactions studied as potential primary mechanisms.
Gene interactions under investigation
- NOS3: eNOS — endothelial NO synthase; proposed upregulation in vascular studies
- VEGFA: Vascular endothelial growth factor; studied in angiogenesis models
- FGF2: Fibroblast growth factor 2; studied in tissue repair context
- EGR1: Early growth response 1; implicated in wound healing cascades
- COX2: Cyclooxygenase-2; anti-inflammatory pathway interactions studied
- MMP1/9: Matrix metalloproteinases; extracellular matrix remodeling research
Amino acid sequence
GEPPPGKPADDAGLV
Full name: Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Research is at preclinical stage with no Phase III human trials completed. Not on the WADA prohibited list as of current guidance — verify current status.
02 · TB-500 Performance & Recovery
Thymosin Beta-4 Fragment (Ac-Ser-Asp-Lys-Pro)
- Molecular weight
- 2,113.34 Da
- Length
- 17 amino acids
- Formula
- C₉₄H₁₄₈N₂₄O₂₄
- Half-life
- ~3 days (estimated)
- Origin
- Thymosin Beta-4 C-terminal fragment
Overview
TB-500 is a synthetic analog of the active region of Thymosin Beta-4 (Tβ4), a 43-amino acid ubiquitous intracellular protein that is one of the most abundant peptides in mammalian cells. The key active fragment is the actin-binding domain — specifically the LKKTET hexapeptide sequence that directly interacts with G-actin.
Mechanism of action — under investigation
The primary mechanism under investigation is G-actin sequestration. Tβ4 and its fragments bind G-actin (monomeric actin) via the LKKTET motif, modulating the equilibrium between G-actin and F-actin (filamentous actin). This affects cell migration, morphology, and wound healing.
Signaling pathways under investigation
- Actin Dynamics (G/F-actin): Direct binding to G-actin via LKKTET motif; modulates actin polymerization equilibrium — central to cell migration
- ILK-Akt/PKB: Integrin-linked kinase interactions studied; downstream Akt phosphorylation and cell survival signaling
- HIF-1α: Hypoxia-inducible factor interactions studied; may promote angiogenesis in hypoxic tissue
- VEGF Upregulation: Secondary to HIF-1α activation; studied in wound healing and angiogenesis models
- NF-κB Modulation: Anti-inflammatory properties studied via NF-κB pathway inhibition in preclinical models
- MMP Expression: Matrix metalloproteinase modulation studied in tissue remodeling research
Receptor interactions
No classical GPCR receptor identified. Primary interaction is direct protein-protein binding with G-actin. ILK serves as a co-receptor/mediator for downstream signaling.
Gene interactions under investigation
- TMSB4X: Thymosin Beta-4 gene — TB-500 is the synthetic active fragment
- ILK: Integrin-linked kinase — studied interaction target
- ACTA1/2: Actin genes — direct binding target via LKKTET motif
- HIF1A: Hypoxia-inducible factor 1-alpha — studied upregulation
- AKT1: Protein kinase B — downstream of ILK interactions
- VEGFA: Angiogenesis research via HIF-1α cascade
Amino acid sequence
Ac-SDKPDMAEIEKTFDKSKLKKTET (active fragment: LKKTET / KLKKTET)
Full name: Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Note: Thymosin Beta-4 and its peptide fragments are on the WADA prohibited list for in-competition use. Athletes must verify current WADA status before any consultation.
03 · GHK-Cu Longevity & Metabolic
Glycyl-L-Histidyl-L-Lysine Copper(II)
- Molecular weight
- 340.38 Da (free peptide) / 402.93 Da (Cu²⁺ complex)
- Length
- 3 amino acids + Cu²⁺
- Formula
- C₁₄H₂₃CuN₆O₄
- Half-life
- ~2 hours (plasma)
- Origin
- Naturally occurring in human plasma, saliva, urine
Overview
GHK-Cu is one of the most extensively studied peptides in longevity and regenerative research, with natural occurrence in human plasma where concentrations decline significantly with age.
Mechanism of action — under investigation
GHK-Cu research focuses on gene expression modulation — microarray studies suggest it may influence over 4,000 human genes — and superoxide dismutase (SOD) activity via the Cu²⁺ complex, potentially reducing oxidative stress.
Signaling pathways under investigation
- TGF-β / SMAD: Stimulates TGF-β1 production; downstream SMAD signaling drives collagen I and III synthesis and ECM remodeling
- SOD Mimetic Activity: Cu²⁺ complex exhibits superoxide dismutase-like activity; may reduce ROS and oxidative stress burden
- NF-κB Inhibition: Anti-inflammatory pathway; studied suppression of NF-κB-driven pro-inflammatory cytokine expression
- VEGF / Angiogenesis: Upregulation of VEGF and FGF2 studied in wound healing and neovascularization research
- p63 / p73 Pathway: Studies suggest interaction with p63 tumor suppressor; proposed anti-oncogenic gene regulation
- Wnt Signaling: Proposed interactions with Wnt pathway in stem cell and tissue regeneration research
Receptor interactions
No single identified receptor. GHK-Cu is thought to act via direct gene expression modulation, enzyme interactions (SOD mimicry), and growth factor stimulation.
Gene interactions under investigation
- COL1A1: Collagen Type I — upregulated in studies; skin and tissue structure
- COL3A1: Collagen Type III — wound healing and ECM remodeling
- TGFB1: TGF-β1 — primary signaling driver in GHK-Cu collagen research
- SOD1/2: Superoxide dismutase — antioxidant pathway interactions
- MMP1: Matrix metalloproteinase 1 — ECM remodeling regulation
- VEGFA: Angiogenesis and wound healing research context
Amino acid sequence
GHK (tripeptide; forms square-planar Cu²⁺ complex via N-terminal amine, imidazole N, and two deprotonated amide nitrogens)
Full name: Gly-His-Lys
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. The copper complex is naturally present in human physiology. Research is at preclinical and early observational stage.
04 · CJC-1295 Longevity & Metabolic
DAC-GRF / Modified GRF(1-29)
- Molecular weight
- 3,367.9 Da (with DAC) / 3,149.6 Da (without DAC)
- Length
- 29 amino acids + Drug Affinity Complex
- Formula
- C₁₄₉H₂₄₆N₄₄O₄₂S
- Half-life
- ~6-8 days (with DAC) / ~30 min (without DAC)
- Origin
- Synthetic GHRH analog
Overview
CJC-1295 is a synthetic analog of GHRH(1-29) with four amino acid substitutions that confer protease resistance, and a Drug Affinity Complex (DAC) modification enabling albumin binding for extended half-life.
Mechanism of action — under investigation
CJC-1295 acts as a full agonist at the GHRH receptor (GHRHR) on somatotroph cells of the anterior pituitary, driving GH secretion via Gαs/cAMP/PKA pathway activation.
Signaling pathways under investigation
- GHRHR / cAMP / PKA: Primary pathway: GHRHR Gαs coupling → adenylyl cyclase → cAMP elevation → PKA activation → GH secretion
- PLC / IP3 / DAG: Secondary: Gαq coupling → PLC activation → IP3 and DAG production → intracellular Ca²⁺ release
- IGF-1 / mTOR: Downstream of GH release: hepatic IGF-1 production → IGF-1R activation → PI3K/Akt/mTOR anabolic signaling
- JAK2 / STAT5: GH receptor signaling: JAK2 phosphorylation → STAT5b activation → IGF-1 gene transcription in liver
- MAPK / ERK: GH receptor downstream: Ras/Raf/MEK/ERK cascade — cell proliferation and differentiation research
- Somatostatin Feedback: GH elevation stimulates somatostatin release from hypothalamus — natural negative feedback modulation
Receptor interactions
Primary: GHRHR (Growth Hormone Releasing Hormone Receptor) — Class B1 GPCR. Albumin binding via DAC modification extends plasma half-life.
Gene interactions under investigation
- GH1: Growth hormone 1 — primary secreted product; pituitary somatotrophs
- IGF1: Insulin-like growth factor 1 — hepatic production downstream of GH
- GHRHR: GHRH receptor — direct binding target of CJC-1295
- SSTR2: Somatostatin receptor 2 — feedback regulation of GH release
- IGF1R: IGF-1 receptor — downstream anabolic signaling
- STAT5B: Signal transducer — GH receptor pathway transcription factor
Amino acid sequence
YADAIFTQSYRKVLAQHSARKLLQDIMSRK-DAC
Full name: Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg
Regulatory & safety status
Not a licensed medicine for the advisory context discussed at The Catalyst Clinic. GH secretagogues including GHRH analogs are on the WADA prohibited list. Mandatory IGF-1 baseline required.
05 · Ipamorelin Longevity & Metabolic
NNC 26-0161
- Molecular weight
- 711.86 Da
- Length
- 5 amino acids
- Formula
- C₃₈H₄₉N₉O₅
- Half-life
- ~2 hours (subcutaneous)
- Origin
- Synthetic GH secretagogue — ghrelin receptor agonist
Overview
Ipamorelin is a selective pentapeptide GHS-R1a agonist. Its key advantage is selectivity — it stimulates GH release without significantly increasing cortisol, prolactin, or ACTH.
Mechanism of action — under investigation
Ipamorelin is a full agonist at GHS-R1a (the ghrelin receptor). Binding activates Gαq/11 coupled phospholipase C, increasing IP3 and DAG, mobilizing intracellular Ca²⁺, and activating PKC — driving GH granule exocytosis.
Signaling pathways under investigation
- GHS-R1a / Gαq / PLC: Primary: GHS-R1a activation → Gαq coupling → PLC-β activation → IP3/DAG → Ca²⁺ mobilization → GH exocytosis
- PKC Activation: DAG production → PKC activation → GH secretory granule trafficking and exocytosis
- Voltage-Gated Ca²⁺ Channels: Ca²⁺ influx via L-type VGCCs — synergistic with IP3-driven Ca²⁺ release
- cAMP / PKA (minor): Minor Gαs coupling contributes to somatotroph activation
- IGF-1 Downstream: GH release → hepatic IGF-1 production → IGF-1R → PI3K/Akt/mTOR anabolic signaling cascade
- GHRH Synergy: Ipamorelin + CJC-1295 combination acts on separate receptors — synergistic amplification of GH pulse amplitude studied
Receptor interactions
Primary: GHS-R1a (Ghrelin Receptor / Growth Hormone Secretagogue Receptor 1a) — Class A GPCR.
Gene interactions under investigation
- GHSR: GHS-R1a gene — ghrelin receptor, direct binding target
- GH1: Growth hormone — secreted product
- IGF1: Downstream hepatic production; anabolic signaling
- PCSK1: Prohormone convertase — GH precursor processing
- SST: Somatostatin — feedback inhibition of GH release
- GHRL: Ghrelin — endogenous GHS-R1a ligand
Amino acid sequence
[Aib¹,His²,D-2-Nal³,D-Phe⁴,Lys⁵]-NH₂
Full name: Aib-His-D-2-Nal-D-Phe-Lys-NH₂
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. On WADA prohibited list. Mandatory IGF-1 baseline required.
06 · Epithalon Longevity & Metabolic
Epitalon / Epithalone / Ala-Glu-Asp-Gly
- Molecular weight
- 390.35 Da
- Length
- 4 amino acids
- Formula
- C₁₄H₂₀N₄O₁₀
- Half-life
- Not established in humans
- Origin
- Synthetic tetrapeptide derived from Epithalamin (pineal gland polypeptide extract)
Overview
Epithalon is a synthetic tetrapeptide originally derived from Epithalamin, a polypeptide fraction isolated from bovine pineal gland extracts. Its primary research focus is telomere biology.
Mechanism of action — under investigation
The primary mechanism under study is telomerase activation. Research suggests Epithalon may upregulate TERT expression, potentially elongating telomeres in aged cells.
Signaling pathways under investigation
- Telomerase / TERT: Proposed upregulation of TERT expression; telomerase activation studied in lymphocyte and somatic cell models
- Epigenetic / Histone Modification: Studies suggest influence on histone H1, H3 acetylation and chromatin structure
- CLOCK / BMAL1 / Circadian: Interactions with core circadian clock proteins studied; proposed restoration of circadian rhythm amplitude
- Melatonin Synthesis: Pineal gland interactions studied; proposed modulation of AANAT and melatonin production
- p53 / Cell Cycle: Studies suggest interactions with p53 pathway; proposed anti-apoptotic effects in non-cancer cells
- Antioxidant Pathways: Reduction in oxidative stress markers studied; superoxide dismutase and catalase activity modulation
Receptor interactions
No classical receptor identified. Proposed mechanisms involve direct nuclear/epigenetic actions.
Gene interactions under investigation
- TERT: Telomerase reverse transcriptase — primary research target
- TERC: Telomerase RNA component — template for telomere elongation
- CLOCK: Circadian clock gene — studied interaction
- BMAL1: ARNTL — core circadian transcription factor
- TP53: p53 tumor suppressor — proposed cytoprotective interactions
- AANAT: Arylalkylamine N-acetyltransferase — melatonin synthesis rate-limiting enzyme
Amino acid sequence
AEDG
Full name: Ala-Glu-Asp-Gly
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Research primarily from Russian literature. Not approved by the MHRA or FDA.
07 · Semax Cognitive & Mood
MEHFPGP-Pro / ACTH(4-7)PGP analog
- Molecular weight
- 813.0 Da
- Length
- 7 amino acids
- Formula
- C₃₇H₅₁N₉O₁₀
- Half-life
- ~20 minutes (intranasal, active CNS window longer)
- Origin
- Synthetic ACTH(4-7) analog with Pro-Gly-Pro extension
Overview
Semax was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences as a nootropic and neuroprotective agent. A synthetic heptapeptide analog of ACTH(4-7) with a stability extension.
Mechanism of action — under investigation
Semax primarily acts by upregulating BDNF expression. It interacts with melanocortin receptors (MC4R > MC3R) in the CNS and may modulate serotonin and dopamine systems.
Signaling pathways under investigation
- BDNF / TrkB: Primary neuroprotective pathway: BDNF upregulation → TrkB receptor activation → PI3K/Akt and MAPK/ERK cell survival signaling
- Melanocortin / MC4R: MC4R agonism in CNS — modulates neuronal excitability and dopaminergic activity
- Dopamine / MAO: Proposed MAO inhibition-adjacent effects; increased dopamine availability in prefrontal cortex in preclinical models
- Serotonin System: 5-HT synthesis and receptor sensitivity modulation studied
- VEGF / Neuroprotection: Upregulation of VEGF studied; proposed neuroprotective via angiogenesis in ischemia models
- Nitric Oxide (CNS): nNOS modulation studied in brain; proposed role in memory consolidation research
Receptor interactions
MC4R (primary CNS target), MC3R (secondary). Does NOT significantly activate MC2R — no steroidogenic effect.
Gene interactions under investigation
- BDNF: Brain-derived neurotrophic factor — primary studied upregulation target
- NTRK2: TrkB receptor — downstream BDNF signaling mediator
- MC4R: Melanocortin 4 receptor — direct interaction studied in CNS
- VEGFA: Neuroprotective angiogenesis in ischemia models
- NGF: Nerve growth factor — studied alongside BDNF in neuroprotection research
- SLC6A4: Serotonin transporter — serotonin system interaction research
Amino acid sequence
MEHFPGP
Full name: Met-Glu-His-Phe-Pro-Gly-Pro
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Pre-consultation diagnostics required.
08 · Selank Cognitive & Mood
TP-7 / Tuftsin analog
- Molecular weight
- 751.86 Da
- Length
- 7 amino acids
- Formula
- C₃₃H₅₇N₁₁O₉
- Half-life
- ~2 minutes (intranasal, active CNS window longer)
- Origin
- Synthetic Tuftsin (TKPR) analog with Gly-Pro-Pro extension
Overview
Selank is based on Tuftsin, a naturally occurring tetrapeptide derived from IgG. The Pro-Gly-Pro extension dramatically increases stability and CNS penetration. More pronounced anxiolytic properties than Semax.
Mechanism of action — under investigation
Primary mechanism under study is GABA-A receptor modulation via a benzodiazepine-independent mechanism. Also demonstrates serotonergic activity and enkephalinase inhibition.
Signaling pathways under investigation
- GABA-A Modulation: Positive allosteric modulation of GABA-A receptor studied; benzodiazepine-independent anxiolytic mechanism
- Enkephalinase Inhibition: Inhibits NEP (neprilysin); extends half-life of Met-enkephalin and Leu-enkephalin
- Serotonin / 5-HT₂: 5-HT₂ receptor interactions studied; serotonergic anxiolytic and mood regulatory activity
- BDNF / TrkB: BDNF upregulation studied; neuroprotective and neuroplasticity pathway activation
- HPA Axis Normalization: Cortisol/ACTH normalization in stress models studied
- IL-6 / Immune Modulation: Derived from Tuftsin — immune system interactions studied
Receptor interactions
GABA-A receptor (allosteric, non-benzodiazepine site); 5-HT₂ serotonin receptors; possible μ-opioid receptor-adjacent effects via enkephalin preservation.
Gene interactions under investigation
- GABRA: GABA-A receptor subunits — studied allosteric modulation sites
- MME: Neprilysin / Enkephalinase — inhibition studied
- BDNF: Neurotrophin — upregulation studied
- HTR2A: 5-HT₂A receptor — serotonergic interaction research
- IL6: Interleukin-6 — immune modulation research
- PENK: Proenkephalin — endogenous opioid peptide system interaction
Amino acid sequence
TKPRPGP
Full name: Thr-Lys-Pro-Arg-Pro-Gly-Pro
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Pre-consultation diagnostics required.
09 · NAD+ Longevity & Metabolic
Nicotinamide Adenine Dinucleotide (oxidized form)
- Molecular weight
- 663.43 Da
- Length
- Dinucleotide coenzyme
- Formula
- C₂₁H₂₇N₇O₁₄P₂
- Half-life
- ~3-5 minutes (plasma)
- Origin
- Endogenous coenzyme in all living cells
Overview
NAD+ is not a peptide but is included as a core longevity research compound. Intracellular NAD+ levels decline with age — estimates suggest 50%+ decline — associated with mitochondrial dysfunction and reduced sirtuin activity.
Mechanism of action — under investigation
NAD+ is consumed by three major enzyme classes: Sirtuins (SIRT1-7), PARPs (DNA damage repair), and CD38/CD157. Restoring NAD+ levels aims to reactivate sirtuin-mediated longevity pathways.
Signaling pathways under investigation
- Sirtuin / SIRT1 / SIRT3: NAD+-dependent deacylases: SIRT1 (mitochondrial biogenesis), SIRT3 (ROS management), SIRT6 (DNA repair)
- PARP1/2 DNA Repair: NAD+ substrate for PARP; consumed during DNA repair
- PGC-1α / Mitochondrial Biogenesis: SIRT1 deacetylates PGC-1α → mitochondrial biogenesis, fatty acid oxidation
- AMPK / mTOR: NAD+/NADH ratio sensed by AMPK; low NAD+ → AMPK activation → autophagy
- p53 / DNA Damage Response: SIRT1 deacetylates p53 → modulates apoptosis vs survival
- CD38 / Calcium Signaling: CD38 produces cADPR from NAD+ → intracellular Ca²⁺ release
Receptor interactions
Not a classical receptor-binding peptide. Acts as substrate/cofactor for SIRT1-7, PARPs, CD38, and the electron transport chain.
Gene interactions under investigation
- SIRT1: Sirtuin 1 — NAD+-dependent deacylase; longevity
- SIRT3: Mitochondrial sirtuin — ROS management
- NAMPT: Rate-limiting enzyme in NAD+ salvage pathway
- PARP1: Major NAD+ consumer during DNA repair
- CD38: NAD+ glycohydrolase — major catabolism enzyme
- PCAF/GCN5: Acetyltransferases regulated downstream of NAD+
Amino acid sequence
AMP ↔ NMN dinucleotide
Full name: Adenine-Ribose-Phosphate-Phosphate-Ribose-Nicotinamide
Regulatory & safety status
Compounded NAD+ is not a licensed medicine under the Human Medicines Regulations 2012. Flushing and cardiovascular symptoms are rate-dependent — slow subcutaneous administration required.
10 · MOTS-c Longevity & Metabolic
Mitochondrial ORF of the 12S rRNA Type-C
- Molecular weight
- 2,174.5 Da
- Length
- 16 amino acids
- Formula
- C₉₄H₁₅₂N₂₆O₂₈S
- Half-life
- Not established; circulating levels measurable in plasma
- Origin
- Encoded in mitochondrial genome (12S rRNA region)
Overview
MOTS-c is encoded within the 12S rRNA gene of the mitochondrial genome. It can translocate to the nucleus under metabolic stress where it acts as a direct transcriptional regulator.
Mechanism of action — under investigation
MOTS-c acts as a metabolic regulator. Under glucose restriction, it translocates to the nucleus, directly interacts with Nrf2 antioxidant response elements, and inhibits the folate cycle activating AMPK indirectly.
Signaling pathways under investigation
- AMPK Activation: Inhibition of folate cycle → AICAR accumulation → AMPK activation
- Nrf2 / ARE: Nuclear translocation → direct Nrf2 binding → antioxidant response activation
- Mitochondrial Biogenesis: AMPK → PGC-1α → mitochondrial biogenesis
- Insulin Sensitivity / GLUT4: AMPK-mediated GLUT4 translocation studied
- Folate Cycle Inhibition: MOTS-c inhibits MTHFD1 → AICAR accumulation → indirect AMPK activation
- Inflammatory Resolution: Anti-inflammatory effects studied via Nrf2/NF-κB crosstalk
Receptor interactions
No classical surface receptor. MOTS-c acts via mitochondria → cytoplasm → nucleus translocation. Nuclear interactions with Nrf2 and ARE sequences.
Gene interactions under investigation
- MT-RNR1: 12S rRNA mitochondrial gene — MOTS-c encoding region
- NFE2L2: Nrf2 — direct nuclear binding target
- PRKAA1/2: AMPK α subunits — indirect activation
- MTHFD1: Methylenetetrahydrofolate dehydrogenase — inhibited by MOTS-c
- PPARGC1A: PGC-1α — downstream of AMPK
- HMOX1: HO-1 / Heme oxygenase-1 — Nrf2 target
Amino acid sequence
MRWQEMGYIFYPRKLR
Full name: Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Very early stage research. Not approved by the MHRA or FDA.
11 · KPV Immune & Gut
Lys-Pro-Val / α-MSH C-terminal tripeptide
- Molecular weight
- 355.43 Da
- Length
- 3 amino acids
- Formula
- C₁₆H₃₁N₄O₄⁺ (protonated)
- Half-life
- Not formally established; very short plasma half-life
- Origin
- C-terminal tripeptide of α-MSH
Overview
KPV is the C-terminal tripeptide of α-MSH. Despite being only three amino acids, KPV retains significant anti-inflammatory and immunomodulatory activity. Its small size enables potential oral bioavailability for gut-targeted applications.
Mechanism of action — under investigation
KPV acts primarily via melanocortin receptors (MC1R on immune cells). MC1R coupling via Gαs drives cAMP elevation and PKA activation, suppressing NF-κB and downstream pro-inflammatory cytokine production.
Signaling pathways under investigation
- MC1R / cAMP / PKA / NF-κB: Primary: MC1R (Gαs) → adenylyl cyclase → cAMP → PKA → NF-κB inhibition → reduced IL-1β, TNF-α, IL-6
- PepT1 (SLC15A1) Transport: Tripeptide transporter-mediated intracellular entry in gut epithelial cells
- MAPK / ERK Inhibition: Proposed inhibition of LPS-stimulated ERK phosphorylation
- NLRP3 Inflammasome: Studies suggest inhibition of NLRP3 inflammasome activation
- Tight Junction Restoration: Gut barrier function research: claudin, occludin, ZO-1 modulation studied
- ROS Scavenging: Antioxidant effects studied; reduction of mitochondrial ROS
Receptor interactions
MC1R (primary), MC3R (secondary). PepT1/SLC15A1 (tripeptide transporter in gut epithelium).
Gene interactions under investigation
- MC1R: Melanocortin 1 receptor — primary immune cell target
- RELA: NF-κB p65 subunit — downstream inhibition
- SLC15A1: PepT1 transporter — KPV uptake into intestinal epithelial cells
- IL1B: IL-1β — suppressed downstream of NF-κB inhibition
- TNFA: TNF-α — pro-inflammatory cytokine suppressed
- CLDN1/OCLN: Claudin-1, Occludin — tight junction proteins
Amino acid sequence
KPV
Full name: Lys-Pro-Val
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. One of the compounds with a stronger preclinical safety profile. Not approved by the MHRA or FDA.
12 · Sermorelin Longevity & Metabolic
GRF(1-29)·NH₂ / Geref
- Molecular weight
- 3,357.9 Da
- Length
- 29 amino acids
- Formula
- C₁₄₉H₂₄₆N₄₄O₄₂S
- Half-life
- ~10-20 minutes (plasma)
- Origin
- Synthetic GHRH(1-29) analog
Overview
Sermorelin closely mirrors the natural GHRH pulse — short half-life mimicking the physiological GHRH pulse pattern. Pulsatility preserves the natural GH/IGF-1 regulatory axis.
Mechanism of action — under investigation
Full agonist at GHRHR on pituitary somatotrophs via Gαs/cAMP/PKA activation driving GH secretion. Short half-life allows pulsatile stimulation rather than sustained elevation.
Signaling pathways under investigation
- GHRHR / Gαs / cAMP / PKA: Primary: GHRHR agonism → Gαs → adenylyl cyclase → cAMP → PKA → GH secretory granule exocytosis
- Ca²⁺ / CaM Kinase: Intracellular Ca²⁺ mobilization contributes to GH exocytosis
- Somatostatin Feedback Preserved: Short half-life allows somatostatin feedback cycle to function normally
- IGF-1 / JAK2 / STAT5b: Downstream: GH → JAK2/STAT5b → IGF-1 gene transcription in liver
- PI3K / Akt / mTOR: IGF-1 downstream signaling → protein synthesis
- MAPK / ERK: GHR downstream: Ras/Raf/MEK/ERK signaling
Receptor interactions
GHRHR (Growth Hormone Releasing Hormone Receptor) — Class B1 GPCR.
Gene interactions under investigation
- GHRHR: GHRH receptor — direct binding target
- GH1: Growth hormone — secreted product
- IGF1: Downstream hepatic production
- SSTR2: Somatostatin receptor 2 — feedback regulation
- GHR: Growth hormone receptor — downstream target
- STAT5B: Transcription factor — GHR signaling
Amino acid sequence
YADAIFTNSYRKVLGQLSARKLLQDIMSR-NH₂
Full name: Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH₂
Regulatory & safety status
Not licensed for the advisory context at The Catalyst Clinic. FDA-approved as Geref for pediatric GH deficiency diagnosis only. On WADA prohibited list. Mandatory IGF-1 baseline required.
13 · Humanin Longevity & Metabolic
HN / Humanin-G (S14G-HN)
- Molecular weight
- 2,687.2 Da
- Length
- 21 amino acids
- Formula
- C₁₁₄H₁₉₃N₃₅O₃₆S
- Half-life
- Not formally established in humans
- Origin
- Encoded in mitochondrial 16S rRNA gene
Overview
Humanin was discovered in 2001 during a screen for genes that suppress neuronal death in Alzheimer's disease models. Encoded within the 16S rRNA gene of the mitochondrial genome, it circulates in plasma and declines with age.
Mechanism of action — under investigation
Humanin protects via: (1) direct BAX binding preventing mitochondrial membrane permeabilization; (2) tripartite receptor complex activation driving JAK2/STAT3 survival signaling; (3) IGFBP3 interaction modulating IGF-1 bioavailability.
Signaling pathways under investigation
- BAX Inhibition / Apoptosis: Direct BAX binding prevents MOMP → cytochrome c retained → caspase cascade blocked
- gp130 / JAK2 / STAT3: CNTFR/WSX-1/gp130 receptor complex → JAK2 → STAT3 → anti-apoptotic gene transcription
- PI3K / Akt / mTOR: FPRL1/CXCR4 activation → PI3K/Akt → mTOR
- IGFBP3 Interaction: Humanin binds IGFBP3 — altered IGF-1 bioavailability studied
- AMPK Activation: Metabolic studies suggest AMPK activation in insulin-sensitive tissues
- Mitochondrial Bioenergetics: Proposed improvement in mitochondrial membrane potential in aging models
Receptor interactions
Tripartite receptor complex: CNTFR/WSX-1/gp130; FPRL1; CXCR4. Intracellular: direct BAX protein-protein interaction.
Gene interactions under investigation
- MT-RNR2: 16S rRNA mitochondrial gene — Humanin encoding region
- BAX: BCL2-associated X protein — direct binding target
- STAT3: Signal transducer — gp130 downstream
- IGFBP3: IGF-binding protein 3 — direct interaction
- BCL2: Anti-apoptotic protein — upregulated downstream of STAT3
- CNTFR: Ciliary neurotrophic factor receptor — tripartite complex component
Amino acid sequence
MAPRGFSCLLLLTSEIDLPVK
Full name: Met-Ala-Pro-Arg-Gly-Phe-Ser-Cys-Leu-Leu-Leu-Leu-Thr-Ser-Glu-Ile-Asp-Leu-Pro-Val-Lys
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Early-stage preclinical research. Not approved by the MHRA or FDA.
14 · Thymosin Alpha-1 Immune & Gut
Tα1 / Zadaxin
- Molecular weight
- 3,108.4 Da
- Length
- 28 amino acids
- Formula
- C₁₂₉H₂₁₅N₃₃O₅₅
- Half-life
- ~2 hours (subcutaneous)
- Origin
- N-terminal fragment of Prothymosin Alpha; isolated from thymic extracts
Overview
Thymosin Alpha-1 has the most established clinical research profile of all immunomodulatory peptides in this list, with approved status in several countries for hepatitis B and C — though this approval does not extend to wellness use.
Mechanism of action — under investigation
Acts as a thymic hormone regulating T-cell maturation. Binds TLR2 and TLR9 on dendritic cells, driving Type I interferon production and Th1 polarization.
Signaling pathways under investigation
- TLR2/9 / NF-κB / IFN-α/β: TLR2 and TLR9 agonism → NF-κB activation → Type I interferon production → Th1 polarization
- T-cell Maturation / CD3/CD4/CD8: Upregulation of T-cell surface markers; IL-2 and IL-2R upregulation
- PI3K / Akt: Immune cell survival signaling
- JAK/STAT (STAT1/STAT4): IFN signaling downstream: STAT1 (antiviral), STAT4 (Th1 polarization)
- NK Cell Activation: Enhanced NK cell cytotoxicity; upregulation of perforin and granzyme B
- Th1/Th2 Balance: Th1 polarization via IL-12 and IFN-γ upregulation
Receptor interactions
TLR2 and TLR9 on innate immune cells. Possible interactions with αvβ3 integrin.
Gene interactions under investigation
- PTMA: Prothymosin Alpha gene — Tα1 is N-terminal fragment
- TLR2: Toll-like receptor 2 — direct binding and activation
- TLR9: Toll-like receptor 9
- IFNA1: Type I interferon alpha — upregulated downstream
- IL2: Interleukin-2 — T-cell proliferation
- TMSB4X: Thymosin-related gene
Amino acid sequence
Ac-SDAAVDTSSEITTKDLKEKKEVEEAN
Full name: Ac-Ser-Asp-Ala-Ala-Val-Asp-Thr-Ser-Ser-Glu-Ile-Thr-Thr-Lys-Asp-Leu-Lys-Glu-Lys-Lys-Glu-Val-Val-Glu-Glu-Ala-Glu-Asn-OH
Regulatory & safety status
Approved as Zadaxin in ~35 countries for specific hepatitis indications — this approval does NOT extend to advisory use at The Catalyst Clinic. Not approved by MHRA or FDA for wellness use.
15 · Dihexa Cognitive & Mood
PNB-0408
- Molecular weight
- 686.84 Da
- Length
- Hexapeptide derivative (angiotensin IV analog)
- Formula
- C₃₈H₅₄N₄O₄
- Half-life
- Not formally established; CNS penetration documented in rodent models
- Origin
- Angiotensin IV analog developed at Washington State University
Overview
Dihexa was developed at Washington State University as an Angiotensin IV analog. In preclinical models it shows high potency in synaptic plasticity research via HGF/c-Met signaling activation.
Mechanism of action — under investigation
Acts primarily via the HGF/c-Met receptor tyrosine kinase system. Research suggests it potentiates HGF signaling and activates synaptogenesis-related pathways. High CNS potency claims require independent replication.
Signaling pathways under investigation
- HGF / c-Met / PI3K / Akt: HGF potentiation → c-Met RTK activation → PI3K/Akt → neuronal survival and synaptic plasticity
- MAPK / ERK (c-Met downstream): c-Met → Ras/Raf/MEK/ERK → neurogenesis and synaptic strengthening
- AT4R / IRAP: LNPEP/IRAP — original proposed Ang IV receptor; cognitive function research
- CREB / BDNF Axis: Downstream of c-Met: CREB phosphorylation → BDNF transcription
- LTP Enhancement: Long-term potentiation studies in hippocampal slices
- Synaptogenesis: Dendritic spine density increase studied in preclinical models
Receptor interactions
c-Met (HGF Receptor Tyrosine Kinase); AT4R/IRAP (LNPEP). Receptor binding data limited.
Gene interactions under investigation
- MET: c-Met receptor tyrosine kinase — primary HGF receptor
- HGF: Hepatocyte growth factor — Dihexa potentiation target
- LNPEP: IRAP / AT4R — angiotensin IV receptor
- CREB1: cAMP response element binding protein
- BDNF: Neurotrophic factor — downstream of CREB
- GRIN2B: NMDA receptor subunit 2B — LTP context
Amino acid sequence
Based on Angiotensin IV with N-terminal Val replaced by hexanoyl group — increases CNS penetration
Full name: Hexanoyl-Tyr-Ile-His-Pro-Phe-NH₂
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Very limited preclinical data. No human safety or efficacy trials completed. Approached with significant caution at The Catalyst Clinic.
16 · Tesamorelin Longevity & Metabolic
TH9507 / Egrifta
- Molecular weight
- 5,135.8 Da
- Length
- 44 amino acids + N-terminal modification
- Formula
- C₂₂₁H₃₆₆N₆₈O₆₇S
- Half-life
- ~26 minutes (plasma)
- Origin
- Full-length synthetic GHRH(1-44) analog with trans-3-hexenoic acid modification
Overview
Tesamorelin has the most substantial human clinical data of all GH secretagogues. FDA-approved as Egrifta for HIV-associated lipodystrophy — this approval does not extend to advisory use.
Mechanism of action — under investigation
Full GHRHR agonist protected from DPPIV degradation. The full 44-AA sequence may provide more complete receptor activation than truncated analogs.
Signaling pathways under investigation
- GHRHR / Gαs / cAMP / PKA: Full GHRHR agonism → Gαs → adenylyl cyclase → cAMP → PKA → GH exocytosis
- GH / IGF-1 / JAK2 / STAT5b: GH release → hepatic IGF-1 → anabolic and metabolic effects
- Lipolysis / Adipose Tissue: FDA-approved indication: GH-mediated lipolysis in visceral adipose tissue
- PI3K / Akt / mTOR: IGF-1 downstream: PI3K → Akt → mTOR
- Somatostatin Axis: GH elevation → somatostatin → GHRHR feedback
- Glucose Metabolism: GH counter-regulatory effects on insulin sensitivity — monitoring required
Receptor interactions
GHRHR — Class B1 GPCR. Full 44-AA GHRH sequence provides maximal receptor engagement.
Gene interactions under investigation
- GHRHR: GHRH receptor — direct binding target
- GH1: Growth hormone — primary secreted product
- IGF1: Downstream anabolic mediator
- LIPE: Hormone-sensitive lipase — FDA-approved indication basis
- DPP4: DPPIV — enzyme protected against by N-terminal modification
- SSTR2: Somatostatin receptor 2 — feedback regulation
Amino acid sequence
Full 44-AA GHRH with N-terminal trans-3-hexenoic acid conjugation protecting DPPIV cleavage
Full name: Trans-3-hexenoic acid-[full 44 AA GHRH sequence]-NH₂
Regulatory & safety status
FDA-APPROVED as Egrifta for HIV-associated lipodystrophy ONLY. This approval does NOT extend to wellness or advisory use. On WADA prohibited list. Mandatory IGF-1 baseline and metabolic monitoring required.
17 · LL-37 Performance & Recovery
hCAP-18(109-140) / CAMP peptide
- Molecular weight
- 4,493.3 Da
- Length
- 37 amino acids
- Formula
- C₂₀₅H₃₄₀N₆₀O₅₃
- Half-life
- ~1-3 hours (plasma)
- Origin
- C-terminal fragment of hCAP-18 (human cathelicidin antimicrobial protein)
Overview
LL-37 is the only member of the cathelicidin family of antimicrobial peptides expressed in humans. Distinctive amphipathic α-helical structure enabling both antimicrobial activity and complex mammalian cell signaling.
Mechanism of action — under investigation
Multiple mechanisms: direct antimicrobial membrane disruption; receptor-mediated FPRL1 signaling on immune cells; EGFR transactivation driving wound-related biology; VEGF-associated angiogenesis research.
Signaling pathways under investigation
- FPRL1 (FPR2) / ERK / PI3K: FPRL1 activation → ERK phosphorylation and PI3K/Akt → immune cell activation
- EGFR Transactivation: Metalloprotease-mediated EGFR ligand shedding → EGFR activation → epithelial biology research
- TLR Modulation: LL-37 modulates TLR2, TLR4, TLR9 — context and concentration dependent
- NLRP3 Inflammasome: Biphasic concentration-dependent effects studied
- P2X7 / Purinergic: Pore-forming activity on mammalian cells at higher concentrations
- Angiogenesis / VEGF: VEGF upregulation studied via FPRL1 and EGFR pathways
Receptor interactions
FPRL1/FPR2; EGFR (via transactivation); P2X7; CXCR2, CXCR4; TLR2, TLR4, TLR9.
Gene interactions under investigation
- CAMP: Cathelicidin antimicrobial peptide — LL-37 encoding gene
- FPR2: FPRL1 — primary signaling receptor
- EGFR: Epidermal growth factor receptor — transactivation target
- VEGFA: Angiogenesis research context
- MMP8: Neutrophil collagenase — MMP activity modulation
- DEFB: Beta-defensins — synergistic antimicrobial peptides
Amino acid sequence
LLGDFFRKSKEKIGKEFKRIVQRIKDFLRNLVPRTES
Full name: Leu-Leu-Gly-Asp-Phe-Phe-Arg-Lys-Ser-Lys-Glu-Lys-Ile-Gly-Lys-Glu-Phe-Lys-Arg-Ile-Val-Gln-Arg-Ile-Lys-Asp-Phe-Leu-Arg-Asn-Leu-Val-Pro-Arg-Thr-Glu-Ser
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Concentration-dependent effects are significant — both pro- and anti-inflammatory activities documented. Caution warranted.
18 · Cerebrolysin Cognitive & Mood
FPF-1070 / Cere
- Molecular weight
- Variable (peptide mixture)
- Length
- Peptide mixture (~15% low-MW peptides, ~85% free amino acids)
- Formula
- Complex mixture
- Half-life
- ~30-60 minutes (plasma)
- Origin
- Enzymatic digest of purified porcine brain proteins
Overview
Cerebrolysin is a complex mixture produced from enzymatic digestion of porcine brain proteins. Extensively researched in Eastern Europe and Asia for neurological applications.
Mechanism of action — under investigation
Acts as a neurotrophic factor mimetic via: BDNF-like TrkB activation; CNTF-like JAK/STAT3 signaling; APP and tau modulation in AD models; Nrf2 antioxidant pathway activation.
Signaling pathways under investigation
- BDNF-like / TrkB / PI3K / Akt: BDNF-mimetic fractions → TrkB RTK activation → PI3K/Akt/mTOR → neuronal survival
- CNTF-like / JAK2 / STAT3: CNTF-mimetic fractions → JAK2/STAT3 → anti-apoptotic gene expression
- MAPK / ERK / CREB: TrkB and CNTFR downstream → CREB phosphorylation → synaptic plasticity
- APP / Tau Modulation: Reduction of APP processing to Aβ studied; tau phosphorylation modulation
- Nrf2 / Antioxidant: Nrf2/ARE antioxidant pathway activation studied
- Calcium Homeostasis: NMDA receptor-mediated Ca²⁺ influx modulation studied
Receptor interactions
TrkB (BDNF receptor RTK), gp130/CNTFR (CNTF receptor complex), p75NTR. Complex mixture — receptor profile reflects mixture activity.
Gene interactions under investigation
- NTRK2: TrkB receptor — BDNF-like fraction target
- STAT3: JAK/STAT signaling — CNTF-like downstream
- MAPT: Tau protein — hyperphosphorylation modulation
- APP: Amyloid precursor protein — Aβ processing research
- NFE2L2: Nrf2 — antioxidant pathway
- ARC: Activity-regulated cytoskeleton-associated protein
Amino acid sequence
Not a single sequence compound. Standardized to consistent biological activity.
Full name: Complex mixture — BDNF-like, CNTF-like, NGF fragments and neuropeptides
Regulatory & safety status
Not approved by MHRA or FDA for advisory use. Approved in some countries for specific neurological indications. Porcine brain origin — theoretical prion risk cited by Western regulatory bodies. Complex mixture presents quality standardization challenges.
19 · VIP Immune & Gut
Vasoactive Intestinal Peptide / VIP₁₋₂₈
- Molecular weight
- 3,326.8 Da
- Length
- 28 amino acids
- Formula
- C₁₄₇H₂₃₇N₄₃O₄₃S
- Half-life
- ~1-2 minutes (plasma)
- Origin
- Endogenous neuropeptide
Overview
VIP is one of the most pleiotropic neuropeptides known — functioning simultaneously as a neurotransmitter, neuromodulator, vasodilator, bronchodilator, and immunomodulator.
Mechanism of action — under investigation
Signals via two high-affinity Class B GPCRs: VPAC1 (ubiquitous) and VPAC2. Both couple to Gαs → adenylyl cyclase → cAMP → PKA, driving immune modulation, vasodilation, and gut function.
Signaling pathways under investigation
- VPAC1/2 / Gαs / cAMP / PKA: Primary: VPAC1 or VPAC2 → Gαs → cAMP → PKA → tissue-specific downstream effects
- MAPK / ERK (secondary): Gβγ-mediated coupling → ERK activation in some cell types
- Treg Induction / IL-10: In dendritic cells: VIP → VPAC1 → cAMP → Treg-inducing cytokine profile
- NF-κB Inhibition: cAMP → PKA → inhibition of IKK → reduced TNF-α, IL-6, IL-12
- Smooth Muscle / cGMP: Vasodilation via cAMP and NO-independent cGMP mechanisms
- CFTR / Chloride Secretion: Intestinal epithelial CFTR activation → Cl⁻ and water secretion
Receptor interactions
VPAC1 (VIPR1) and VPAC2 (VIPR2) — Class B GPCRs, Gαs-coupled.
Gene interactions under investigation
- VIP: Vasoactive intestinal peptide gene
- VIPR1: VPAC1 receptor — ubiquitous expression
- VIPR2: VPAC2 receptor — brain, pancreas, muscle
- FOXP3: Treg transcription factor — upregulated downstream
- IL10: IL-10 — immunosuppressive cytokine
- CFTR: Cystic fibrosis transmembrane conductance regulator
Amino acid sequence
HSDAVFTDNYTRLRKQMAVKKYLNSILN-NH₂
Full name: His-Ser-Asp-Ala-Val-Phe-Thr-Asp-Asn-Tyr-Thr-Arg-Leu-Arg-Lys-Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Asn-Ser-Ile-Leu-Asn-NH₂
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Extremely short plasma half-life makes systemic delivery challenging. Not approved by MHRA or FDA for wellness context.
20 · MK-677 Longevity & Metabolic
Ibutamoren / Ibutamoren Mesylate / L-163,191
- Molecular weight
- 624.77 Da (free base) / 776.96 Da (mesylate salt)
- Length
- Non-peptide small molecule GHS-R1a agonist
- Formula
- C₂₈H₄₀N₄O₄S
- Half-life
- ~24 hours (oral)
- Origin
- Synthetic non-peptide GH secretagogue — Merck Research Laboratories
Overview
MK-677 is unique as a non-peptide small molecule — orally bioavailable (~60-70%) with a ~24-hour half-life. Completed Phase II trials for muscle wasting. Most clinically studied oral GH secretagogue.
Mechanism of action — under investigation
Full agonist at GHS-R1a via Gαq/PLC/IP3/Ca²⁺ mechanism. 24-hour half-life results in sustained GH elevation — distinction from pulsatile peptide secretagogues.
Signaling pathways under investigation
- GHS-R1a / Gαq / PLC / Ca²⁺: Full GHS-R1a agonism → Gαq → PLC-β → IP3/DAG → Ca²⁺ + PKC → GH exocytosis
- Hypothalamic Appetite / NPY: GHS-R1a in hypothalamus → NPY/AgRP → appetite increase — significant side effect consideration
- IGF-1 / JAK2 / STAT5b: Sustained GH → hepatic IGF-1 → anabolic signaling
- Insulin Resistance Risk: Prolonged GH elevation → peripheral insulin resistance — fasting glucose monitoring required
- Sleep Architecture / REM: MK-677 shown to increase REM and slow-wave sleep in clinical studies
- Cortisol / Prolactin (minimal): Minimal cortisol or prolactin elevation at research doses — selectivity advantage
Receptor interactions
GHS-R1a (Ghrelin Receptor) — high-affinity full agonist (Ki ~1 nM). Oral bioavailability ~60-70%.
Gene interactions under investigation
- GHSR: GHS-R1a gene — direct high-affinity binding target
- GH1: Growth hormone — sustained elevation with 24h half-life
- IGF1: Downstream hepatic production
- NPY: Neuropeptide Y — hypothalamic appetite stimulation
- INS: Insulin — reduced sensitivity; glucose monitoring required
- DPP4: DPPIV — does NOT degrade MK-677 (non-peptide advantage)
Amino acid sequence
Not a peptide. Orally bioavailable GHS-R1a agonist binding same site as ghrelin.
Full name: N/A — non-peptide small molecule
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by MHRA or FDA. On WADA prohibited list. Clinically significant side effects: water retention, increased appetite, potential insulin resistance. Mandatory metabolic panel, fasting glucose, and IGF-1 baseline required.
21 · L-Glutathione Longevity & Metabolic
GSH / γ-L-Glutamyl-L-Cysteinylglycine (reduced)
- Molecular weight
- 307.32 Da
- Length
- 3 amino acids (tripeptide)
- Formula
- C₁₀H₁₇N₃O₆S
- Half-life
- ~10 minutes (plasma, reduced form)
- Origin
- Endogenous tripeptide synthesized in all human cells
Overview
L-Glutathione is the body's principal intracellular antioxidant tripeptide, distinguished by an unusual gamma-peptide bond between glutamate and cysteine that resists standard peptidase cleavage. Intracellular levels decline with age and under oxidative or detoxification burden. Note: oral and parenteral glutathione have very different bioavailability, and systemic supplementation raising intracellular GSH is contested.
Mechanism of action — under investigation
Glutathione functions as the primary redox buffer via the GSH/GSSG cycle. It is the cofactor for glutathione peroxidases (neutralizing peroxides) and glutathione-S-transferases (Phase II conjugation of xenobiotics and heavy metals). It regenerates vitamins C and E and maintains protein thiol status.
Signaling pathways under investigation
- GSH/GSSG Redox Cycle: Central intracellular redox buffer; reduced GSH oxidized to GSSG neutralizing ROS, regenerated by glutathione reductase (NADPH-dependent)
- Glutathione Peroxidase (GPx): Cofactor for GPx1-4; reduction of hydrogen peroxide and lipid peroxides
- Glutathione-S-Transferase (Phase II): Conjugation of electrophiles, xenobiotics, and heavy metals for excretion — detoxification pathway
- Nrf2 / ARE: GSH status influences Nrf2 antioxidant response element signaling
- Vitamin C/E Regeneration: Recycles oxidized ascorbate and tocopherol back to active antioxidant forms
- Mercapturic Acid Pathway: GSH conjugates processed to mercapturic acids for renal excretion — relevant to heavy-metal clearance
Receptor interactions
Not a receptor-binding peptide. Acts as enzyme cofactor and direct redox agent. Membrane transport via specific GSH transporters; extracellular breakdown/resynthesis via the gamma-glutamyl cycle (GGT).
Gene interactions under investigation
- GCLC: Glutamate-cysteine ligase catalytic subunit — rate-limiting synthesis enzyme
- GSS: Glutathione synthetase — second synthesis step
- GPX1: Glutathione peroxidase 1 — primary peroxide-neutralizing enzyme
- GSR: Glutathione reductase — regenerates reduced GSH from GSSG
- GSTP1: Glutathione-S-transferase P1 — Phase II conjugation
- NFE2L2: Nrf2 — master antioxidant transcription factor influenced by redox status
Amino acid sequence
ECG (non-standard γ-linkage between glutamate and cysteine)
Full name: γ-Glu-Cys-Gly
Regulatory & safety status
Glutathione is a naturally occurring compound available as a supplement in many jurisdictions. Compounded IV/injectable glutathione is not a licensed medicine under the Human Medicines Regulations 2012 for wellness use. Oral bioavailability for raising intracellular GSH is scientifically contested; precursors (NAC, glycine) are often studied instead. Not approved by MHRA or FDA for the advisory context.
22 · Pentadeca Arginate Performance & Recovery
PDA / Arginate salt of BPC-157 analog (15-mer)
- Molecular weight
- ~1,600 Da (arginate salt form; base peptide ~1,419 Da)
- Length
- 15 amino acids + arginate salt
- Formula
- Not standardized across suppliers
- Half-life
- Not established in humans
- Origin
- Synthetic BPC-157-related pentadecapeptide, arginate-salt formulated
Overview
Pentadeca Arginate (PDA) is a marketing-driven variant of BPC-157, formulated as an arginate salt and promoted as a more stable successor. It has almost no independent published characterization — the great majority of claims are extrapolated from BPC-157 research rather than direct PDA studies. Buyer- and formulation-dependent; composition is not standardized.
Mechanism of action — under investigation
Proposed mechanisms are extrapolated from BPC-157: nitric oxide system modulation, angiogenesis via VEGF, and cytoprotective effects. The added arginine (arginate) is claimed to support NO substrate availability. No PDA-specific mechanistic studies of quality exist to date.
Signaling pathways under investigation
- NO/eNOS (extrapolated): Proposed via BPC-157 backbone plus arginine as NO substrate — not directly demonstrated for PDA
- VEGF / Angiogenesis (extrapolated): Assumed from BPC-157 tissue-repair research; no PDA-specific data
- FAK-Paxillin (extrapolated): Cell migration pathway assumed from parent compound
- Growth Factor Modulation (extrapolated): Proposed but unverified for the arginate formulation
Receptor interactions
No identified receptor. Mechanism inferred entirely from BPC-157; PDA-specific receptor data does not exist.
Gene interactions under investigation
- NOS3: eNOS — proposed via BPC-157 mechanism and arginine substrate
- VEGFA: Extrapolated angiogenesis target
- FGF2: Extrapolated tissue-repair context
- EGR1: Wound-healing cascade — extrapolated from BPC-157
Amino acid sequence
BPC-157 backbone as arginate salt (GEPPPGKPADDAGLV + arginate)
Full name: Related to BPC-157 pentadecapeptide backbone (Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val), arginate-conjugated
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Critically: PDA has minimal independent characterization — nearly all claims are extrapolated from BPC-157. Composition is not standardized between suppliers. Should be treated as an uncharacterized research compound.
23 · AOD-9604 Longevity & Metabolic
hGH Fragment 176-191 / Tyr-hGH(177-191)
- Molecular weight
- 1,815.1 Da
- Length
- 16 amino acids
- Formula
- C₈₇H₁₄₄N₂₆O₂₅
- Half-life
- Short (minutes, plasma)
- Origin
- Synthetic C-terminal fragment of human growth hormone with N-terminal tyrosine
Overview
AOD-9604 is the C-terminal fragment of human growth hormone (residues 176-191) plus an N-terminal tyrosine, developed as an anti-obesity agent intended to promote lipolysis without the growth or insulin-resistance effects of full GH. Clinical obesity trials did not meet primary weight-loss endpoints.
Mechanism of action — under investigation
Proposed to stimulate lipolysis and inhibit lipogenesis via a mechanism independent of the GH receptor — possibly β3-adrenergic-adjacent effects on adipocytes. It does not raise IGF-1 and does not appear to affect blood glucose in the way full GH does.
Signaling pathways under investigation
- Lipolysis / β3-Adrenergic (proposed): Proposed stimulation of fat oxidation in adipocytes without GH receptor involvement
- Lipogenesis Inhibition: Studied reduction of new fat synthesis in adipose tissue
- HSL / Hormone-Sensitive Lipase: Proposed activation of lipolytic enzyme cascade
- No IGF-1 Elevation: Distinguishing feature: does not activate hepatic IGF-1 axis — no anabolic/hypertrophic signaling
Receptor interactions
No high-affinity receptor definitively identified. Does NOT act via the GH receptor. Proposed β3-adrenergic-adjacent adipocyte effects.
Gene interactions under investigation
- GH1: Source protein — AOD-9604 is a C-terminal fragment
- LIPE: Hormone-sensitive lipase — proposed lipolytic target
- ADRB3: β3-adrenergic receptor — proposed adipocyte pathway
- PLIN1: Perilipin — lipid droplet regulation in lipolysis
Amino acid sequence
YLRIVQCRSVEGSCGF (hGH 177-191 + N-terminal Tyr)
Full name: Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Failed to meet primary endpoints in Phase II obesity trials. Holds a limited food-additive/GRAS-adjacent status in some jurisdictions but is NOT MHRA or FDA approved as a weight-loss therapeutic. On WADA prohibited list (GH fragment).
24 · FOXO4-DRI Longevity & Metabolic
FOXO4 D-Retro-Inverso peptide / proxofim
- Molecular weight
- ~5,200 Da (D-retro-inverso 47-mer)
- Length
- ~47 amino acids (D-retro-inverso)
- Formula
- Complex; D-amino acid retro-inverso construct
- Half-life
- Not established in humans
- Origin
- Engineered D-retro-inverso peptide derived from the FOXO4-p53 interaction domain
Overview
FOXO4-DRI is an experimental senolytic peptide designed to disrupt the FOXO4-p53 interaction inside senescent cells, releasing p53 to the mitochondria and triggering apoptosis selectively in senescent cells. Notoriety comes from a single influential 2017 mouse study. Human safety and efficacy data are essentially absent.
Mechanism of action — under investigation
FOXO4-DRI competitively interferes with FOXO4 binding to p53 in senescent cells. Freed p53 relocates to mitochondria, initiating intrinsic apoptosis preferentially in senescent (not healthy) cells — the definition of a senolytic.
Signaling pathways under investigation
- FOXO4-p53 Disruption: Core mechanism: blocks FOXO4-p53 complex → nuclear-excluded p53 → mitochondrial p53 → apoptosis in senescent cells
- Intrinsic Apoptosis / BAX-BAK: Mitochondrial p53 → BAX/BAK activation → cytochrome c release → caspase cascade
- Senescence-Associated Secretory Phenotype (SASP): Senescent-cell clearance proposed to reduce SASP inflammatory burden
- p16 / p21 Senescence Markers: Reduction studied in aged tissue following senescent-cell clearance in mouse models
Receptor interactions
No cell-surface receptor. Cell-penetrating construct enters cells and acts via intracellular protein-protein interaction disruption (FOXO4-p53).
Gene interactions under investigation
- FOXO4: Forkhead box O4 — direct interaction target
- TP53: p53 — released to mitochondria to trigger apoptosis
- CDKN2A: p16INK4a — senescence marker
- CDKN1A: p21 — senescence/cell-cycle marker
- BAX: Pro-apoptotic effector downstream of mitochondrial p53
Amino acid sequence
D-amino acid retro-inverso construct — engineered, not a natural sequence
Full name: D-retro-inverso analog of the FOXO4 DNA-binding/p53-interaction region, fused to a cell-penetrating (TAT-derived) sequence
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by any regulator anywhere. Evidence base is essentially one 2017 mouse study; NO human safety, dosing, or efficacy data exists. Triggering p53-mediated apoptosis systemically carries theoretical risks. Treated as a purely experimental compound with no clinical basis.
25 · Kisspeptin Longevity & Metabolic
Kisspeptin-10 / Metastin fragment / KP-54
- Molecular weight
- 1,302.5 Da (Kisspeptin-10)
- Length
- 10 amino acids (KP-10); parent KP-54 is 54 AA
- Formula
- C₆₃H₈₃N₁₇O₁₄ (KP-10)
- Half-life
- ~4 minutes (KP-10, plasma) / ~28 min (KP-54)
- Origin
- Endogenous neuropeptide encoded by KISS1; hypothalamic reproductive regulator
Overview
Kisspeptin is the master upstream regulator of the reproductive hormonal axis, acting on the hypothalamus to stimulate GnRH release. It has a genuine and growing human clinical research base in reproductive medicine — distinct from most compounds on this list. KP-10 is the active C-terminal decapeptide.
Mechanism of action — under investigation
Kisspeptin binds KISS1R (GPR54) on GnRH neurons → Gαq/PLC → IP3/Ca²⁺ → GnRH secretion → downstream LH and FSH release from the pituitary → gonadal sex-hormone production. It is the key gatekeeper of pubertal onset and reproductive function.
Signaling pathways under investigation
- KISS1R (GPR54) / Gαq / PLC: Primary: KISS1R activation → Gαq → PLC-β → IP3/DAG → Ca²⁺ → GnRH neuron depolarization and GnRH release
- GnRH / LH / FSH Axis: GnRH release → pituitary gonadotroph LH and FSH secretion → gonadal steroidogenesis
- HPG Axis Regulation: Master upstream control of the hypothalamic-pituitary-gonadal axis
- ERK / MAPK: Secondary KISS1R signaling via ERK phosphorylation
- Metastasis Suppression (KISS1): Original discovery context: KISS1 as a metastasis-suppressor gene
Receptor interactions
KISS1R (GPR54) — Class A GPCR, Gαq-coupled. Expressed on hypothalamic GnRH neurons.
Gene interactions under investigation
- KISS1: Kisspeptin gene — encodes the parent peptide
- KISS1R: GPR54 — kisspeptin receptor, direct binding target
- GNRH1: GnRH — downstream secreted product
- LHB: LH beta subunit — pituitary downstream
- FSHB: FSH beta subunit — pituitary downstream
- TAC3: Neurokinin B — co-regulator in KNDy neurons
Amino acid sequence
YNWNSFGLRF-NH₂ (Kisspeptin-10, C-terminal decapeptide)
Full name: Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂ (KP-10)
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012 for wellness use. Notably has a legitimate and expanding human clinical trial base in reproductive medicine and IVF contexts. Not MHRA or FDA approved for the advisory context. Effects on the reproductive axis require endocrine oversight.
26 · Follistatin Performance & Recovery
FST / FS-344 / Activin-binding protein
- Molecular weight
- ~31,000-38,000 Da (glycoprotein isoforms)
- Length
- 288-315 amino acids (FST-288 / FST-315 isoforms)
- Formula
- Glycoprotein — not a small peptide
- Half-life
- Variable by isoform; FST-315 longer via heparin/cell-surface binding
- Origin
- Endogenous glycoprotein; myostatin and activin antagonist
Overview
Follistatin is an endogenous glycoprotein that binds and neutralizes TGF-β superfamily members — most notably myostatin and activin. Because myostatin brakes muscle growth, follistatin is heavily promoted for muscle hypertrophy. It is a large glycoprotein, not a peptide, and is most often pursued as gene therapy through unregulated channels. CRITICAL: driving myostatin blockade in a patient with cardiomyopathy is a serious theoretical hazard.
Mechanism of action — under investigation
Follistatin binds myostatin (GDF-8) and activin A with high affinity, preventing them from engaging ActRIIB and releasing the SMAD2/3 brake on muscle growth. This de-represses muscle protein synthesis and satellite-cell activity.
Signaling pathways under investigation
- Myostatin / ActRIIB / SMAD2/3: Core: follistatin sequesters myostatin → blocks ActRIIB → removes SMAD2/3 growth inhibition → muscle hypertrophy
- Activin A Neutralization: Binds activin A — affects reproduction, inflammation, and fibrosis pathways broadly
- Follistatin/GDF-11: Binds GDF-11 — aging and cardiac biology implications (bidirectional, contested)
- mTOR / Protein Synthesis: Downstream de-repression of anabolic muscle protein synthesis
- TGF-β Superfamily Modulation: Broad interference across the TGF-β/activin/BMP signaling family — off-target breadth is the risk
Receptor interactions
Not a receptor agonist. Acts as a soluble ligand trap, binding myostatin/activin/GDF-11 and preventing receptor (ActRIIB) engagement.
Gene interactions under investigation
- FST: Follistatin gene — the compound itself
- MSTN: Myostatin (GDF-8) — primary neutralization target
- INHBA: Activin A subunit — high-affinity binding target
- ACVR2B: ActRIIB — receptor blocked downstream of myostatin sequestration
- GDF11: GDF-11 — bound by follistatin; aging/cardiac relevance
- SMAD3: Downstream transcription factor de-repressed
Amino acid sequence
Not a short synthetic peptide — full glycoprotein or gene-therapy product
Full name: Large multi-domain glycoprotein (N-terminal + three follistatin domains)
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by any regulator for muscle growth or wellness. Most commonly offered as gene therapy via unregulated overseas clinics with thin human safety data. SAFETY: myostatin/activin blockade broadly suppresses the TGF-β system; driving muscle-hypertrophy signaling is contraindicated on first principles in patients with hypertrophic cardiomyopathy or structural heart disease. On WADA prohibited list. Requires cardiology gating; not appropriate to present as clinic-ready.
27 · ACE-031 Performance & Recovery
ActRIIB-Fc / Ramatercept (soluble activin receptor trap)
- Molecular weight
- ~78,000-80,000 Da (Fc-fusion dimer)
- Length
- Recombinant Fc-fusion protein (ActRIIB extracellular domain + IgG1 Fc)
- Formula
- Recombinant fusion protein — not a peptide
- Half-life
- ~10-15 days (Fc-fusion, extended)
- Origin
- Engineered soluble ActRIIB extracellular domain fused to IgG1 Fc
Overview
ACE-031 is a soluble decoy receptor: the extracellular domain of ActRIIB fused to an antibody Fc region. It mops up myostatin, activins, and other ActRIIB ligands before they reach the real receptor, driving muscle growth. Development was HALTED in Duchenne muscular dystrophy trials due to safety signals — notably vascular/bleeding-related adverse events.
Mechanism of action — under investigation
As a ligand trap, ACE-031 binds myostatin, activin A/B, GDF-11 and related ActRIIB ligands in circulation, preventing SMAD2/3 signaling and de-repressing muscle growth — broader ligand capture than follistatin.
Signaling pathways under investigation
- ActRIIB Ligand Trap: Sequesters myostatin, activin A/B, GDF-11 → blocks ActRIIB → removes SMAD2/3 muscle-growth brake
- SMAD2/3 De-repression: Downstream muscle protein synthesis increase
- Activin / Vascular Effects: Off-target activin/BMP capture implicated in the vascular adverse events (epistaxis, telangiectasia) that halted trials
- GDF-11 / Erythropoiesis: ActRIIB ligand capture affects red-cell and vascular biology
- BMP Pathway Crosstalk: Broad TGF-β/BMP superfamily interference — source of off-target risk
Receptor interactions
Not a receptor agonist. Soluble decoy receptor (ActRIIB-Fc) that captures circulating ligands.
Gene interactions under investigation
- ACVR2B: ActRIIB — the receptor whose decoy domain forms ACE-031
- MSTN: Myostatin — primary captured ligand
- INHBA: Activin A — captured; linked to vascular side effects
- GDF11: GDF-11 — captured; erythropoietic/vascular relevance
- SMAD2: Downstream signaling de-repressed
- ENG: Endoglin — vascular TGF-β context relevant to bleeding effects
Amino acid sequence
Not a peptide — recombinant receptor-Fc fusion (decoy receptor)
Full name: ActRIIB extracellular domain fused to human IgG1 Fc — recombinant fusion protein
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by any regulator. Clinical development was DISCONTINUED after trials showed vascular safety signals including epistaxis (nosebleeds) and telangiectasia from off-target effects on blood vessels. SAFETY: the documented bleeding-related vascular effects make this especially hazardous alongside anticoagulant therapy, and the myostatin-blockade hypertrophy signaling is contraindicated in structural heart disease. On WADA prohibited list. Not appropriate as a clinic-offered compound.
28 · Testagen Longevity & Metabolic
Testagen / Ala-Glu-Asp-Leu peptide bioregulator
- Molecular weight
- ~446 Da
- Length
- 4 amino acids (tetrapeptide)
- Formula
- C₁₉H₃₀N₄O₉ (approximate)
- Half-life
- Not established in humans
- Origin
- Synthetic Khavinson-type peptide bioregulator (Russian research lineage)
Overview
Testagen is a short synthetic "peptide bioregulator" from the Khavinson family of Russian-developed tetrapeptides, promoted for reproductive/endocrine support and gonadal function. As with the broader Khavinson bioregulator class, the evidence base is almost entirely Russian-language, small, and not independently replicated to Western standards.
Mechanism of action — under investigation
Proposed to act as a peptide bioregulator influencing gene expression in reproductive/endocrine tissue — the Khavinson class hypothesis is that short peptides bind DNA/regulatory regions to modulate tissue-specific protein synthesis. Mechanistic evidence is weak and largely uncorroborated outside the originating research group.
Signaling pathways under investigation
- Gene Expression Modulation (proposed): Khavinson bioregulator hypothesis: short peptides influence tissue-specific transcription — weakly evidenced
- Reproductive/Endocrine Tissue (proposed): Promoted for gonadal/reproductive support; direct data limited
- Antioxidant Effects (proposed): General claims across the peptide-bioregulator class
Receptor interactions
No identified receptor. Proposed direct nuclear/epigenetic action per the peptide-bioregulator hypothesis — not independently validated.
Gene interactions under investigation
- (unspecified): Khavinson-class peptides propose direct DNA/regulatory interaction but specific validated gene targets are not established
Amino acid sequence
AEDL
Full name: Ala-Glu-Asp-Leu
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Evidence base is almost entirely Russian-language and not independently replicated. Should be treated as an uncharacterized research compound with minimal quality human data.
29 · SS-31 Longevity & Metabolic
Elamipretide / MTP-131 / Bendavia
- Molecular weight
- 639.79 Da
- Length
- 4 amino acids
- Formula
- C₃₂H₄₉N₉O₅
- Half-life
- ~2-4 hours (plasma, subcutaneous)
- Origin
- Synthetic mitochondria-targeting Szeto-Schiller (aromatic-cationic) tetrapeptide
Overview
SS-31 is an aromatic-cationic tetrapeptide from the Szeto-Schiller series that concentrates in the inner mitochondrial membrane independently of membrane potential and binds the phospholipid cardiolipin. Cardiolipin integrity declines with age and disease. SS-31 has one of the more substantial human clinical programmes on this list — Phase II/III trials in heart failure, ischemia-reperfusion, primary mitochondrial myopathy and Barth syndrome — though pivotal efficacy results have been mixed.
Mechanism of action — under investigation
SS-31 selectively associates with cardiolipin in the inner mitochondrial membrane, stabilizing cristae architecture and protecting the cytochrome c–cardiolipin interaction. This improves electron transport chain coupling and ATP synthesis efficiency while reducing mitochondrial reactive oxygen species and cardiolipin peroxidation.
Signaling pathways under investigation
- Cardiolipin Binding: Selective association with cardiolipin in the inner mitochondrial membrane; stabilizes cristae curvature and respiratory supercomplex assembly
- Electron Transport Chain: Preserves the cytochrome c–cardiolipin interaction; improves Complex I–IV coupling and ATP synthesis efficiency
- ROS Reduction: Reduces mitochondrial superoxide and cardiolipin peroxidation; lowers oxidative-stress burden
- Mitochondrial Permeability Transition: Studied inhibition of mPTP opening; preserves membrane potential under ischemic stress
- Cristae Ultrastructure: Restoration of cristae morphology studied in aged and diseased mitochondria
- Apoptosis / Cytochrome c: Retention of cytochrome c reduces caspase activation in ischemia-reperfusion models
Receptor interactions
No cell-surface receptor. SS-31 acts intracellularly via direct biophysical association with cardiolipin in the inner mitochondrial membrane; cellular uptake and mitochondrial accumulation are membrane-potential independent.
Gene interactions under investigation
- CRLS1/PGS1: Cardiolipin synthase / phosphatidylglycerophosphate synthase — cardiolipin is the direct binding target
- TAZ: Tafazzin — cardiolipin remodeling enzyme; central to the Barth syndrome trials
- CYCS: Cytochrome c — interaction preserved by cardiolipin stabilization
- OPA1: Cristae/fusion protein — mitochondrial ultrastructure research
- SOD2: Manganese superoxide dismutase — oxidative-stress context
- PPARGC1A: PGC-1α — mitochondrial biogenesis; downstream functional studies
Amino acid sequence
D-Arg-Dmt-Lys-Phe-NH₂ (aromatic-cationic; Dmt = 2′,6′-dimethyltyrosine)
Full name: D-Arg-2′,6′-dimethyl-Tyr-Lys-Phe-NH₂
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Has an unusually substantial human clinical trial base (Phase II/III in heart failure, mitochondrial myopathy and Barth syndrome) but pivotal efficacy endpoints have been mixed. Verify current WADA status before any consultation.
30 · Oxytocin Cognitive & Mood
OT / cyclic nonapeptide neurohormone
- Molecular weight
- 1,007.19 Da
- Length
- 9 amino acids (cyclic nonapeptide)
- Formula
- C₄₃H₆₆N₁₂O₁₂S₂
- Half-life
- ~3-5 minutes (plasma); longer central effect window
- Origin
- Endogenous hypothalamic neuropeptide, released from the posterior pituitary
Overview
Oxytocin is a nine-amino-acid cyclic neuropeptide synthesized in the paraventricular and supraoptic nuclei of the hypothalamus and released from the posterior pituitary. Classically known for uterine contraction and milk ejection, it is extensively studied as a central modulator of social bonding, trust, anxiety and the stress response. It differs from vasopressin by only two residues, which underlies cross-reactivity at vasopressin receptors.
Mechanism of action — under investigation
Oxytocin signals via the oxytocin receptor (OXTR), a Class A GPCR coupled to Gαq/11 → phospholipase C-β → IP3/DAG → intracellular Ca²⁺ mobilization, driving smooth-muscle contraction peripherally. Centrally, it modulates amygdala reactivity and interacts with dopaminergic and serotonergic reward circuitry.
Signaling pathways under investigation
- OXTR / Gαq / PLC: Primary: OXTR activation → Gαq/11 → PLC-β → IP3/DAG → Ca²⁺ mobilization → smooth-muscle contraction and neuronal signaling
- Amygdala Modulation: Central OXTR signaling studied to attenuate amygdala threat reactivity — anxiolytic and prosocial effects
- Dopamine / Reward: Interaction with mesolimbic dopamine studied in pair-bonding and social-reward research
- HPA Axis: Modulation of the cortisol/ACTH stress response studied
- MAPK / ERK: Secondary OXTR coupling → ERK activation in some tissues
- eNOS / Vasodilation: OXTR on endothelium studied; nitric-oxide-mediated cardiovascular effects
Receptor interactions
OXTR (oxytocin receptor) — primary. Cross-reacts with vasopressin receptors (AVPR1A, AVPR1B, AVPR2) at higher concentrations owing to close structural homology.
Gene interactions under investigation
- OXT: Oxytocin/neurophysin I precursor gene
- OXTR: Oxytocin receptor — direct binding target, Class A GPCR
- AVPR1A: Vasopressin V1a receptor — cross-reactivity due to structural similarity
- CD38: Regulates hypothalamic oxytocin release; social-behavior research
- TH: Tyrosine hydroxylase — dopaminergic reward-circuit interaction
- FOS: c-Fos — neuronal activation marker in oxytocin studies
Amino acid sequence
CYIQNCPLG-NH₂ (intramolecular Cys1–Cys6 disulfide bond)
Full name: Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH₂ (Cys1–Cys6 disulfide bridge)
Regulatory & safety status
Oxytocin is a licensed medicine for obstetric indications (labor induction, postpartum hemorrhage) — this approval does NOT extend to the wellness, social or advisory context discussed at The Catalyst Clinic. Intranasal and off-label behavioural use is investigational and not MHRA or FDA approved for those purposes.
31 · Pinealon Cognitive & Mood
EDR / Glu-Asp-Arg (Khavinson tripeptide bioregulator)
- Molecular weight
- 418.4 Da
- Length
- 3 amino acids (tripeptide)
- Formula
- C₁₅H₂₆N₆O₈
- Half-life
- Not established in humans
- Origin
- Synthetic Khavinson-type peptide bioregulator (brain/pineal-directed)
Overview
Pinealon is a short synthetic tripeptide from the Khavinson family of Russian-developed peptide bioregulators, promoted for neuroprotection and cognitive support. The class hypothesis holds that very short peptides penetrate the cell and nucleus and modulate tissue-specific gene expression. As with the wider bioregulator class, the evidence base is predominantly Russian-language, small, and not independently replicated to Western standards.
Mechanism of action — under investigation
Proposed to penetrate cells and interact with DNA/chromatin to modulate expression of genes governing neuronal survival, antioxidant defense and resistance to glutamate/hypoxia-induced apoptosis. Originating-group preclinical studies report reduced oxidative stress and protection in hypoxic/ischemic neuronal models. Mechanistic evidence is weak outside the source group.
Signaling pathways under investigation
- Gene Expression Modulation (proposed): Khavinson hypothesis: EDR penetrates the nucleus and influences tissue-specific transcription — weakly evidenced
- Antioxidant / ROS (proposed): Reduction of reactive oxygen species and lipid peroxidation studied in neuronal models
- Anti-Apoptotic (proposed): Protection against glutamate excitotoxicity and hypoxia-induced apoptosis studied preclinically
- Caspase-3 Modulation: Reduced caspase-3 activation reported in originating-group neuronal studies
- Circadian / Pineal (proposed): Pineal-directed bioregulator class; proposed circadian and melatonin-adjacent effects
Receptor interactions
No identified receptor. Proposed direct intracellular/nuclear (epigenetic) action per the peptide-bioregulator hypothesis — not independently validated.
Gene interactions under investigation
- (tissue-specific, unvalidated): Khavinson-class peptides propose direct chromatin interaction; specific validated gene targets are not independently established
- CASP3: Caspase-3 — reduced activation reported in neuronal apoptosis models
- SOD1/GPX1: Antioxidant enzymes — proposed upregulation in oxidative-stress studies
- BDNF: Neurotrophic factor — proposed neuroprotective context (limited data)
Amino acid sequence
EDR
Full name: Glu-Asp-Arg
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Evidence base is almost entirely Russian-language and not independently replicated. Should be treated as an uncharacterized research compound with minimal quality human data.
32 · PT-141 Cognitive & Mood
Bremelanotide / Vyleesi
- Molecular weight
- 1,025.2 Da
- Length
- 7 amino acids (cyclic heptapeptide)
- Formula
- C₅₀H₆₈N₁₄O₁₀
- Half-life
- ~2-3 hours (plasma)
- Origin
- Synthetic cyclic melanocortin agonist; active metabolite lineage of Melanotan II
Overview
PT-141 is a cyclic heptapeptide melanocortin-receptor agonist derived from the Melanotan II lineage, developed for sexual dysfunction. Unlike vasodilator approaches, it acts centrally via the CNS melanocortin system rather than the peripheral vascular pathway. It is FDA-approved as Vyleesi for acquired hypoactive sexual desire disorder in premenopausal women — this approval does NOT extend to the general wellness/advisory context.
Mechanism of action — under investigation
Non-selective melanocortin-receptor agonist with primary activity at MC4R (and secondary MC3R, MC1R). Hypothalamic MC4R activation (Gαs → cAMP → PKA) modulates dopaminergic pathways governing sexual arousal, independent of the nitric-oxide vascular pathway.
Signaling pathways under investigation
- MC4R / Gαs / cAMP / PKA: Primary: hypothalamic MC4R agonism → Gαs → adenylyl cyclase → cAMP → PKA → central arousal signaling
- Dopaminergic Modulation: MC4R activation studied to increase dopamine release in the medial preoptic area — central sexual arousal
- MC3R Signaling: Secondary melanocortin engagement; energy-balance and inflammation research
- MC1R Signaling: Peripheral melanocortin activity — transient flushing and pigmentation-adjacent effects
- Appetite / Energy Balance: MC4R is a central satiety hub — melanocortin research context
- Blood Pressure: Transient increases in blood pressure documented — melanocortin-mediated; monitoring relevant
Receptor interactions
MC4R (primary), MC3R and MC1R (secondary). Does not significantly activate MC2R (adrenal/steroidogenic).
Gene interactions under investigation
- MC4R: Melanocortin 4 receptor — primary CNS target
- MC3R: Melanocortin 3 receptor — secondary target
- MC1R: Melanocortin 1 receptor — peripheral pigmentation/flushing effects
- POMC: Proopiomelanocortin — endogenous melanocortin precursor
- TH: Tyrosine hydroxylase — dopaminergic arousal pathway
- AGRP: Agouti-related peptide — endogenous MC4R antagonist
Amino acid sequence
Ac-Nle-cyclo(Asp-His-D-Phe-Arg-Trp-Lys)-OH (lactam-cyclized heptapeptide)
Full name: Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-OH
Regulatory & safety status
FDA-APPROVED as Vyleesi (bremelanotide) for acquired hypoactive sexual desire disorder in premenopausal women ONLY. This approval does NOT extend to general wellness or advisory use. Not a licensed medicine under the Human Medicines Regulations 2012 for the context discussed. Documented transient blood-pressure elevation and nausea — blood-pressure monitoring relevant.
33 · Vilon Immune & Gut
KE / Lys-Glu (Khavinson dipeptide bioregulator)
- Molecular weight
- 275.30 Da
- Length
- 2 amino acids (dipeptide)
- Formula
- C₁₁H₂₁N₃O₅
- Half-life
- Not established in humans
- Origin
- Synthetic Khavinson-type peptide bioregulator (thymus/immune-directed)
Overview
Vilon is the shortest of the Khavinson peptide bioregulators — a dipeptide (Lys-Glu) promoted for immune modulation, tissue regeneration and anti-aging. The class hypothesis holds that very short peptides enter the nucleus and bind DNA regulatory regions to influence tissue-specific gene expression. As with the wider bioregulator class, the evidence base is predominantly Russian-language, small, and not independently replicated to Western standards.
Mechanism of action — under investigation
Proposed to act as a gene-regulatory dipeptide — modeling studies from the originating group suggest KE can associate with DNA minor-groove/promoter regions and modulate expression of genes involved in immune function, cell proliferation and antioxidant defense. Mechanistic evidence is limited and largely uncorroborated outside the source group.
Signaling pathways under investigation
- Gene Expression Modulation (proposed): Khavinson hypothesis: KE dipeptide binds DNA regulatory regions and influences tissue-specific transcription — weakly evidenced
- Immune / Thymic (proposed): Promoted for T-cell and immune bioregulation; proposed thymic-directed activity
- Antioxidant (proposed): Reduction of oxidative-stress markers reported in originating-group studies
- Cell Proliferation / Telomere (proposed): Proposed effects on fibroblast proliferation and replicative lifespan in cell models
Receptor interactions
No identified receptor. Proposed direct intracellular/nuclear (epigenetic) action per the peptide-bioregulator hypothesis — not independently validated.
Gene interactions under investigation
- (tissue-specific, unvalidated): Khavinson-class dipeptides propose direct DNA/promoter interaction; specific validated gene targets are not independently established
- IL2: Interleukin-2 — proposed immune-bioregulation context
- SOD1/CAT: Antioxidant enzymes — proposed upregulation
- TERT: Telomerase — proposed replicative-lifespan effects (limited data)
Amino acid sequence
KE
Full name: Lys-Glu
Regulatory & safety status
Not a licensed medicine under the Human Medicines Regulations 2012. Not approved by the MHRA or FDA. Evidence base is almost entirely Russian-language and not independently replicated. Should be treated as an uncharacterized research compound with minimal quality human data.
What We Consult On
Areas of Research Interest
Our advisory consultations span the primary domains of peptide compound research. Each area is approached through the lens of your individual biomarker data.
- Tissue repair and musculoskeletal recovery research
- Metabolic and mitochondrial pathway investigation
- Neurological and cognitive signaling research
- Longevity and biological aging pathways
- Immune modulation and gut health research
- Hormonal optimization and endocrine support
- Sleep architecture and recovery biology
- Skin, hair, and aesthetic-related research
Published Works
Literature by Dr. Ethan
Three published works grounded in nearly two decades of peptide research — written to give patients and practitioners the scientific context behind this rapidly evolving field.

Book One
Exploring the World of Peptides
A comprehensive guide to the multifaceted role of peptides in biology, medicine, fitness, and skincare. Beginning with the fundamentals — what peptides are and how they differ from amino acids and proteins — it explores their applications across therapeutic medicine, performance and recovery, and anti-aging skin health, alongside the synthesis methods behind them. 397 pages · published January 2025.

Book Two
Peptide-Based Cancer Therapies
An exploration of the innovative role of peptides in cancer treatment and their potential for targeted therapies with reduced toxicity. Covers hormone analogs, somatostatin analogs, peptide vaccines, peptide-drug conjugates, cell-penetrating and anti-angiogenic peptides, and diagnostic peptides in tumor imaging — closing with the field's challenges and future directions. 95 pages · published January 2025.

Book Three
The Peptide Encyclopedia
The definitive guide to the science and clinical application of peptides — the body's own molecular messengers that heal, regulate, and rejuvenate. Tracing the field from the discovery of insulin to designer peptides like BPC-157, Epithalon, and MOTS-C, it features an A–Z reference of 50 key therapeutic peptides with molecular structure, mechanisms, and dosing. 463 pages · published June 2026.
Reading any of these works before your consultation is encouraged — an informed patient is always a better-served patient.
Dr. Ethan Hausman-Marquis
PhD, Cell & Genomic Biology
- PhD in Cell and Genomic Biology
- US board-certified in regenerative medicine
- European board-certified in longevity medicine
- GMC, European & US-registered doctors
- Member and Faculty of the International Peptide Society
- Member of the European Peptide Society
- Member and Fellow of The American Academy of Anti-Aging Medicine (A4M)
- Almost 20 years peptide research experience
- Three published books in the field
- Host of the renowned podcast, The Science of Ageless Living
The Doctor
Your Peptide Doctor in London
"Every patient deserves a consultation grounded in their own biology — not a template, not an algorithm, and never a recommendation made without data."
Dr. Ethan Hausman-Marquis is the peptide doctor who leads The Catalyst Clinic in London — one of the world's leading peptide researchers and the only internationally published peptide doctor practicing in London. With a PhD in Cell and Genomic Biology and nearly two decades of specialist research, he personally oversees every consultation at The Catalyst Clinic.
His approach is defined by scientific rigor and radical transparency: mandatory diagnostics, personal review of every result, and continuous clinical oversight throughout your program.
Our London Clinic
Our Clinic in Kensington
In-person consultations take place at 96 Kensington High Street, London W8 — a few minutes' walk from High Street Kensington Underground station.
4.9
Rated 4.9 out of 5 from 50 patient reviews on Google.
Common Questions
Frequently Asked Questions
Clear answers on how our advisory consultations work, the regulatory status of the compounds discussed, and what to expect at every stage.
It is a doctor-led private medical advisory consultation focused on the current scientific literature surrounding research peptide compounds, interpreted in the context of your individual biomarker data. Peptides are short chains of amino acids that function as signaling molecules. Most compounds discussed are subjects of ongoing research and are not licensed medicines.
Consultations begin with mandatory bloodwork and are personally overseen by Dr. Ethan Hausman-Marquis. No program is discussed without your data.
No. The compounds referenced are research compounds. They are not licensed medicines under the Human Medicines Regulations 2012 for any therapeutic, wellness, longevity, or aesthetic use discussed at The Catalyst Clinic. A small number hold licences elsewhere for narrow, specific indications; those licences do not extend to this context.
Discussions occur within a regulated private advisory consultation. Where clinically appropriate, a GMC-registered doctor may exercise prescribing discretion; any compounds are dispensed independently by GMP-certified compounding pharmacies, not by the clinic itself. No efficacy claims are made.
It depends on the specific compound and how it is handled. Most research peptides are not licensed medicines. Supplying unlicensed medicinal products is restricted under the Human Medicines Regulations 2012, and medicinal claims for unlicensed products cannot be advertised to the public (ASA/MHRA rules).
The Catalyst Clinic operates as a private medical advisory clinic with consultations by registered doctors. It does not sell or dispense compounds. Patients should understand the regulatory status. Competitive athletes must check the current WADA prohibited list.
Responsible advisory work requires individual data. Without a clear picture of your biomarkers, medical history, and relevant factors, no appropriate personalized discussion can take place.
Every consultation begins with comprehensive bloodwork (60+ biomarkers in London, included in the fee). DEXA body composition scanning is also included in London. Results are reviewed personally by the consulting doctor. This diagnostics-first approach is a core clinical standard.
Safety evidence varies widely between compounds. A few have more human data in specific licensed contexts; many have limited or mainly preclinical evidence. Some compounds have had clinical development stopped over safety signals. This is why bloodwork precedes any discussion and monitoring continues throughout a program.
Mild effects reported in the literature can include injection-site reactions, temporary water retention or appetite changes, or headaches. Serious adverse effects are possible, especially with poor-quality products, improper use, or in people with contraindications. The clinic screens for contraindications and interactions. Advisory consultations are not suitable for everyone. No safety or efficacy guarantees are made.
It is a doctor-led advisory clinic with mandatory comprehensive bloodwork and personal physician review of every result before any program is discussed. Protocols are fully personalized (no templates). Optional genetic/genomic testing with counseling is available. Ongoing monthly doctor reviews and repeat bloodwork every 4–5 months are standard.
Compounds (when accessed) come exclusively from GMP-certified, EMA-regulated or FDA-registered compounding pharmacies with certificates of analysis. The approach emphasizes scientific rigor, transparency about research status, and regulatory alignment rather than product sales. Dr. Ethan Hausman-Marquis (PhD in Cell and Genomic Biology, nearly 20 years of peptide research, three published books) personally oversees consultations.
He is the founder and lead physician. He holds a PhD in Cell and Genomic Biology, has nearly two decades of specialist peptide research experience, is US board-certified in regenerative medicine and European board-certified in longevity medicine, and is a member of the International Peptide Society and A4M.
He has published three books on peptides and hosts the podcast The Science of Ageless Living. He personally reviews diagnostics and oversees advisory programs at the London clinic and remotely.
Programs start from £600 per month. The initial consultation is £200. In London, bloodwork and DEXA scanning are included in the monthly fee. For remote patients, diagnostics are additional and arranged via partner labs. Optional genetic testing is priced separately.
Typical inclusions are a data-driven advisory protocol, personal diagnostic review, monthly reviews, and full written documentation. Exact costs depend on the individualized program. No outcomes are guaranteed.
It starts with mandatory diagnostics. The consulting physician reviews the results personally and discusses relevant areas of peptide research in the context of your data, history, medications, and goals. A documented personalized advisory protocol is developed if appropriate.
This is followed by induction, monthly reviews, and periodic repeat bloodwork. Full transparency about research status and the regulatory framework is provided, along with informed consent covering the advisory nature of the service.
All answers are provided for general information only and follow ASA/CAP and MHRA principles. Nothing here constitutes medical advice, a diagnosis, or a treatment recommendation. Full compliance statement →
Begin
Book a Peptide Consultation in London
Every journey at The Catalyst Clinic begins the same way: with your data. Book an initial consultation and take the first step toward a doctor-led advisory program that is 100% personalized to you — always.
What's Included
- Bespoke advisory protocol
- Bloodwork of 60+ biomarkers (London only)
- DEXA body composition scanning (London only)
- Bespoke AM/PM complete supplementation program from an EMA-Regulated compounding pharmacy
- Personal review of your diagnostics
- A personalized prescribed peptide protocol
- Monthly reviews included
- Full written documentation
96 Kensington High Street
London W8 4SG
+44 20 7801 6347
Also New York · Monaco · Remote worldwide
The Catalyst Clinic operates within a fully regulated private medical framework. Compounds referenced on this website are research compounds and are not licensed medicines under the Human Medicines Regulations 2012. Nothing on this website constitutes medical advice, diagnosis, or a treatment recommendation. All consultations are advisory and conducted by registered doctors. Genetic testing is provided as accredited clinical diagnostic testing with counseling included.

