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A plain-English reference for every compound we carry — with the backstory of who discovered it, how it works at the molecular level, and the peer-reviewed literature behind it. Written for researchers and curious readers alike. Nothing here constitutes medical or dosing guidance.

18 compounds · 18 citations
Longevity & Cognitive

Admax

The neurotrophic research peptide.

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In Plain English

Admax is a synthetic peptide studied in laboratory models for its effects on nerve-growth signaling. Interest centers on whether it can support the survival and branching of neurons — the cellular groundwork behind learning and memory in animal research.

Discovery & Backstory

A more recent entrant to the research-peptide catalog, Admax emerged from work on small neurotrophic sequences designed to mimic fragments of nerve growth factor while remaining small enough to synthesize reliably and cross biological barriers in preclinical models.

Mechanism of Action

Investigated for interaction with NGF-related receptor pathways and downstream markers of synaptic plasticity, including dendritic branching and neurotransmitter-receptor density in cultured neurons and rodent models.

Studied In

  • NGF-pathway and neurotrophic signaling
  • Synaptic-plasticity and memory-formation models
  • Neuroprotection under oxidative stress
Blends

Blend BPC-157 + TB-500

The classic tissue-repair reference blend.

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In Plain English

This blend combines two of the most-studied peptides in preclinical tissue-repair research. BPC-157 is investigated for its effects on the gut, tendons, and vasculature; TB-500 is studied for cell migration and cardiac repair. Researchers use them together to study complementary signaling.

Discovery & Backstory

The pairing emerged organically from the peptide-research community throughout the 2010s as parallel study of both compounds — one from Sikirić's group in Croatia, the other from Goldstein's group in the US — showed distinct but compatible repair pathways.

Mechanism of Action

BPC-157 supports angiogenic signaling and growth-factor upregulation at injury sites; TB-500 promotes cell migration and cytoskeletal reorganization. In preclinical research they engage separate but converging repair pathways.

Studied In

  • Comparative and combined tissue-repair signaling
  • Angiogenesis + cell-migration crosstalk
  • Preclinical injury-recovery models
Blends

Blend CJC-1295 no DAC + Ipamorelin

The GHRH + ghrelin-receptor reference pair.

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In Plain English

This pairs a GHRH analog (CJC-1295 no DAC) with a selective ghrelin-receptor agonist (Ipamorelin). Researchers study this combination because the two peptides act on different pituitary pathways that naturally work together to release growth hormone.

Discovery & Backstory

The GHRH + GHS pairing has been a research staple since Cyril Bowers demonstrated in the 1980s that GHRH and GH-releasing peptides act synergistically on the pituitary. This blend became the canonical modern version of that pairing.

Mechanism of Action

CJC no-DAC activates the GHRH receptor while Ipamorelin activates the ghrelin (GHS-R1a) receptor. Simultaneous activation of both pathways produces a larger, more physiologic GH pulse than either alone in preclinical studies.

Studied In

  • Synergistic somatotroph activation
  • Pulsatile GH-release pharmacology
  • Comparative GHRH + GHS receptor studies
Healing & Recovery· Body Protection Compound 157

BPC-157

The gut-derived repair peptide.

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In Plain English

BPC-157 is a short chain of 15 amino acids originally identified in human gastric juice. In preclinical models it is one of the most studied peptides for tissue repair — tendons, ligaments, muscle, and gut lining — because it appears to help the body's existing healing machinery work faster and more completely.

Discovery & Backstory

Isolated in the early 1990s by Croatian researcher Predrag Sikirić and colleagues at the University of Zagreb, BPC-157 was identified as a fragment of a larger 'body protection compound' naturally present in the stomach. Decades of animal studies followed, catalogued across hundreds of PubMed entries.

Mechanism of Action

In animal models BPC-157 has been observed to modulate the nitric oxide pathway, upregulate growth-factor receptors (particularly VEGFR2), and support new blood-vessel formation (angiogenesis) around injured tissue. This appears to accelerate the recruitment of fibroblasts and the deposition of collagen at wound sites.

Studied In

  • Tendon, ligament, and muscle-repair signaling
  • Gastrointestinal-lining and ulcer models
  • Angiogenesis and vascular repair
  • Neuroprotective pathway studies

Molecular Data

Formula:
C62H98N16O22
MW:
1419.53 g/mol
Length:
15 aa
CAS:
137525-51-0
Sequence:
GEPPPGKPADDAGLV

Peer-Reviewed Citations

  1. Stable gastric pentadecapeptide BPC 157: novel therapy in gastrointestinal tract
    Sikiric P, et al. · Curr Pharm Des · 2011 · PMID 21443489
  2. BPC 157 accelerates healing of transected rat Achilles tendon
    Krivic A, et al. · J Orthop Res · 2006 · PMID 16960916
  3. Cytoprotective effect of BPC 157 on ulcerative colitis in rats
    Sikiric P, et al. · Eur J Pharmacol · 2013 · PMID 23994171
Growth & Performance· Modified GRF (1-29)

CJC-1295 no DAC

The short-acting GHRH analog.

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In Plain English

CJC-1295 (no DAC) is a synthetic version of the first 29 amino acids of GHRH — the hormone your hypothalamus sends to the pituitary to trigger growth-hormone release. Small modifications make it more stable than natural GHRH while preserving the body's natural pulsatile release pattern.

Discovery & Backstory

Developed at ConjuChem in the 2000s. The 'no DAC' version omits the drug-affinity-complex linker of its long-acting sibling, giving researchers a shorter-acting analog for studying pulsatile GH release.

Mechanism of Action

Binds the GHRH receptor on pituitary somatotrophs, stimulating natural GH release in physiologic pulses. Its short half-life means downstream signaling closely mirrors the body's own rhythm.

Studied In

  • Pulsatile GH release and pituitary-axis signaling
  • IGF-1 modulation and downstream growth pathways
  • Somatotroph pharmacology

Molecular Data

Formula:
C152H252N44O42
MW:
3367.9 g/mol
Length:
29 aa

Peer-Reviewed Citations

  1. GHRH analogs and pulsatile growth hormone release
    Teichman SL, et al. · J Clin Endocrinol Metab · 2006 · PMID 16537685
Growth & Performance· CJC-1295 DAC / Modified GRF (1-29) + DAC

CJC-1295 with DAC

The long-acting GHRH analog.

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In Plain English

CJC-1295 with DAC is the same 29-amino-acid GHRH fragment as its 'no DAC' sibling, but with a Drug Affinity Complex attached. That linker lets the peptide bind reversibly to albumin in the blood, so it circulates for days instead of minutes — giving researchers a sustained-signal tool rather than a short pulse.

Discovery & Backstory

Developed at ConjuChem in the early 2000s as part of a program to extend the half-life of peptide drugs by tethering them to serum albumin. It became a standard comparator in preclinical growth-hormone-axis literature precisely because its long action isolates sustained-versus-pulsatile signaling.

Mechanism of Action

Binds the GHRH receptor on pituitary somatotrophs. The DAC linker forms a covalent bond with albumin's Cys34 residue, extending half-life to roughly six to eight days in animal models and producing an elevated GH and IGF-1 baseline rather than discrete pulses.

Studied In

  • Sustained vs. pulsatile GH-axis signaling
  • IGF-1 baseline elevation studies
  • Albumin-binding half-life extension pharmacology
Healing & Recovery· Copper Tripeptide-1

GHK-Cu

The copper peptide behind skin science.

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In Plain English

GHK-Cu is a naturally occurring three-amino-acid peptide bound to a copper ion. It circulates in plasma and drops sharply as we age. In laboratory research it is one of the most studied peptides for skin quality, collagen production, and dermal renewal.

Discovery & Backstory

Discovered by Dr. Loren Pickart in 1973 while studying why older serum failed to support liver-tissue growth as effectively as young serum. He isolated the tripeptide-copper complex and traced its regenerative activity to this small molecule.

Mechanism of Action

GHK-Cu appears to upregulate genes associated with tissue remodeling and antioxidant defense, stimulate fibroblast production of collagen and glycosaminoglycans, and modulate copper-dependent enzymes involved in wound repair.

Studied In

  • Dermal remodeling and collagen synthesis
  • Antioxidant and anti-inflammatory signaling
  • Hair-follicle and stem-cell studies
  • Gene-expression profiling of aging skin

Molecular Data

Formula:
C14H24N6O4·Cu
MW:
402.92 g/mol
Length:
3 aa
CAS:
89030-95-5
Sequence:
GHK

Peer-Reviewed Citations

  1. GHK peptide as a natural modulator of multiple cellular pathways in skin regeneration
    Pickart L, et al. · Biomed Res Int · 2015 · PMID 26236730
  2. GHK-Cu increases collagen and glycosaminoglycan synthesis
    Maquart FX, et al. · FEBS Lett · 1988 · PMID 3181439
Other Peptides

GLOW

The dermal-signaling reference blend.

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In Plain English

GLOW combines GHK-Cu, BPC-157, and TB-500 — three peptides individually studied in dermal-remodeling and collagen-synthesis research. It is a comparative reference blend for laboratory work on skin-quality and dermal-matrix pathways.

Discovery & Backstory

The blend follows from decades of parallel research on each component: Pickart's copper-peptide work, Sikirić's BPC-157 studies, and Goldstein's TB-4 program. Researchers use it as a single reference for studying convergent dermal signaling.

Mechanism of Action

GHK-Cu drives collagen and glycosaminoglycan synthesis; BPC-157 supports angiogenic and growth-factor signaling; TB-4 modulates cell migration and inflammation. In preclinical research they engage complementary dermal-repair pathways.

Studied In

  • Convergent dermal-matrix signaling
  • Collagen and GAG synthesis
  • Angiogenesis-driven skin research
Other Peptides· Mitochondrial ORF of the 12S rRNA-c

MOTS-C

The peptide encoded inside your mitochondria.

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In Plain English

MOTS-c is remarkable because it isn't encoded in the nucleus of the cell like most proteins — it's encoded directly in mitochondrial DNA. This makes it a signal from the mitochondria to the rest of the cell about energy status.

Discovery & Backstory

Discovered in 2015 by Changhan David Lee and Pinchas Cohen at USC. Its identification opened an entirely new class of peptides — mitochondrial-derived peptides — that suggest mitochondria communicate biochemically with the nucleus.

Mechanism of Action

MOTS-c appears to activate AMPK, the cellular energy sensor, promoting glucose uptake and mitochondrial biogenesis. In animal models it has been shown to improve insulin sensitivity and mimic some effects of exercise at the metabolic level.

Studied In

  • AMPK activation and metabolic signaling
  • Insulin sensitivity in aging models
  • Mitochondrial-nuclear crosstalk
  • Exercise-mimetic pathway research

Molecular Data

Formula:
C74H119N23O16S
MW:
1626.94 g/mol
Length:
16 aa
Sequence:
MRWQEMGYIFYPRKLR

Peer-Reviewed Citations

  1. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis
    Lee C, et al. · Cell Metab · 2015 · PMID 25738459
Sexual & Mood· Melanotan II

Melanotan 2

The melanocortin-receptor pigmentation peptide.

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In Plain English

Melanotan II is a synthetic analog of α-MSH — the hormone that tells melanocytes in your skin to produce pigment. It's been widely studied in melanocortin-receptor pharmacology and skin-pigmentation research.

Discovery & Backstory

Developed at the University of Arizona in the 1980s by Victor Hruby and Mac Hadley as a research tool for melanocortin-receptor pharmacology. Related work in the same lab eventually produced PT-141.

Mechanism of Action

Non-selectively agonizes multiple melanocortin receptors, most notably MC1R (in melanocytes, driving eumelanin production) and MC4R (in the CNS, influencing appetite and arousal pathways).

Studied In

  • Melanocortin-receptor subtype pharmacology
  • Melanogenesis and MC1R signaling
  • Appetite and CNS melanocortin research

Molecular Data

Formula:
C50H69N15O9
MW:
1024.18 g/mol
Length:
7 aa
CAS:
121062-08-6

Peer-Reviewed Citations

  1. Melanocortin peptides and receptors in the CNS
    Wikberg JE, et al. · Pharmacol Res · 2000 · PMID 10727425
Longevity & Cognitive· Nicotinamide Adenine Dinucleotide

NAD+

The cellular energy coenzyme.

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In Plain English

NAD+ isn't a peptide — it's a coenzyme every cell in your body uses to run metabolism. Its levels drop steadily with age, which is why it has become one of the most-studied molecules in longevity research over the past two decades.

Discovery & Backstory

First isolated in 1906 by Harden and Young while studying fermentation. Its central role in cellular metabolism earned multiple Nobel Prizes across the 20th century. Modern interest surged after David Sinclair's lab at Harvard published on NAD's connection to sirtuins and aging.

Mechanism of Action

Serves as a coenzyme for hundreds of redox reactions and is a required substrate for sirtuins (SIRT1-7), PARPs, and CD38 — all involved in DNA repair, mitochondrial biogenesis, and inflammatory signaling. Restoring NAD+ levels appears to reactivate these pathways in aged tissue.

Studied In

  • Sirtuin activation and gene-expression studies
  • Mitochondrial biogenesis
  • DNA-repair and PARP research
  • Age-related metabolic-decline models

Molecular Data

Formula:
C21H27N7O14P2
MW:
663.43 g/mol
CAS:
53-84-9

Peer-Reviewed Citations

  1. NAD+ intermediates: the biology and therapeutic potential of NMN and NR
    Rajman L, et al. · Cell Metab · 2018 · PMID 29514064
Sexual & Mood· The 'bonding' peptide

Oxytocin

The social-bonding hormone.

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In Plain English

Oxytocin is a nine-amino-acid peptide made in the hypothalamus and released by the pituitary. It's most famous for its role in childbirth and social bonding — but its receptor is found throughout the brain, gut, heart, and immune system.

Discovery & Backstory

Isolated by Sir Henry Dale in 1906 and later synthesized by Vincent du Vigneaud in 1953 — earning him the Nobel Prize in Chemistry, as it was the first polypeptide hormone ever synthesized. Modern research has vastly expanded its known roles beyond reproduction.

Mechanism of Action

Activates the oxytocin receptor (OXTR), a G-protein coupled receptor, in the brain (amygdala, hypothalamus, nucleus accumbens) and peripheral tissues. Downstream effects include modulation of stress signaling, social-recognition circuits, and smooth-muscle contraction.

Studied In

  • Social-cognition and bonding research
  • HPA-axis and stress-response modulation
  • Autism-spectrum and prosocial-behavior studies

Molecular Data

Formula:
C43H66N12O12S2
MW:
1007.19 g/mol
Length:
9 aa
CAS:
50-56-6
Sequence:
CYIQNCPLG

Peer-Reviewed Citations

  1. Oxytocin and social bonding
    Feldman R · Trends Cogn Sci · 2012 · PMID 22406290
Weight Management· GLP-1 / GIP / Glucagon Triple Agonist (formerly Retatrutide)

GMR-3 RT

The triple receptor next-generation agonist.

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In Plain English

GMR-3 RT takes the twincretin idea one step further: it activates three receptors — GLP-1, GIP, and glucagon — simultaneously. The addition of glucagon activity is intended to raise energy expenditure alongside the appetite and glucose effects of the other two.

Discovery & Backstory

Originally introduced by Eli Lilly as retatrutide in Phase 2 trials published in the New England Journal of Medicine in 2023. It represents the current cutting edge of the 'poly-agonist' class first proposed by endocrinologist Matthias Tschöp.

Mechanism of Action

Simultaneous activation of GLP-1 and GIP amplifies incretin-driven insulin and satiety pathways, while controlled glucagon-receptor activity engages hepatic energy expenditure and lipid mobilization.

Studied In

  • Triple-agonist receptor pharmacology
  • Energy-expenditure and thermogenic signaling
  • Hepatic-fat and liver-metabolism studies
  • Comparative efficacy vs. single/dual agonists

Molecular Data

Formula:
C221H343N51O64
MW:
4731.53 g/mol
Length:
39 aa
CAS:
2381089-83-2

Peer-Reviewed Citations

  1. Triple hormone receptor agonist retatrutide for obesity — a phase 2 trial
    Jastreboff AM, et al. · N Engl J Med · 2023 · PMID 37356241
Longevity & Cognitive· TP-7

Selank

The Russian anxiolytic heptapeptide.

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In Plain English

Selank is a seven-amino-acid analog of tuftsin — a natural immune peptide — modified with additional amino acids for stability. It was developed as a research tool for studying anxiety-related brain signaling without traditional benzodiazepine mechanisms.

Discovery & Backstory

Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences in the 1990s. Alongside Semax, Selank is part of the Russian 'regulatory peptide' research tradition that pursued small brain-active peptides as targeted alternatives to classical CNS drugs.

Mechanism of Action

In animal models Selank appears to increase brain-derived neurotrophic factor (BDNF) expression, modulate GABAergic tone, and influence serotonin turnover — producing anxiolytic-like effects in behavioral models without the sedation or dependence profile of benzodiazepines.

Studied In

  • GABAergic and BDNF signaling
  • Anxiolytic behavioral models
  • Immune-nervous system crosstalk

Molecular Data

Formula:
C33H57N11O9
MW:
751.87 g/mol
Length:
7 aa
CAS:
129954-34-3
Sequence:
TKPRPGP

Peer-Reviewed Citations

  1. The anxiolytic effect of the synthetic peptide Selank
    Kozlovskii II, Danchev ND · Neurosci Behav Physiol · 2003 · PMID 14535158
Longevity & Cognitive· ACTH (4-10) analog

Semax

The Russian nootropic heptapeptide.

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In Plain English

Semax is a seven-amino-acid peptide based on a fragment of ACTH (adrenocorticotropic hormone), but engineered without the hormonal activity. It has been widely studied in Russia for cognitive-pathway signaling and neuroprotective research.

Discovery & Backstory

Developed in the 1980s at Moscow State University by Ivan Ashmarin's group as part of the same regulatory-peptide program that produced Selank. It has been in continuous research use in Russia for decades.

Mechanism of Action

In animal models Semax appears to upregulate BDNF and nerve growth factor (NGF), influence dopamine and serotonin turnover, and modulate the melanocortin system — producing pro-cognitive and neuroprotective signals across multiple pathways.

Studied In

  • BDNF and NGF gene-expression studies
  • Ischemic and neurodegenerative preclinical models
  • Attention and cognitive-behavior research

Molecular Data

Formula:
C37H51N9O10S
MW:
813.92 g/mol
Length:
7 aa
CAS:
80714-61-0
Sequence:
MEHFPGP

Peer-Reviewed Citations

  1. The heptapeptide Semax: neuroprotective and cognitive-enhancing properties
    Ashmarin IP, et al. · Neurosci Behav Physiol · 1997 · PMID 9353786
Healing & Recovery· Thymosin Beta-4

TB-500

The wound-healing peptide from the thymus.

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In Plain English

TB-500 is a synthetic form of Thymosin Beta-4, a peptide naturally produced in nearly every cell in the body but concentrated in wound fluid and platelets. In animal research it has been studied for how it supports cell migration to injury sites — essentially helping cells 'find' the wound and start rebuilding.

Discovery & Backstory

Thymosin Beta-4 was first isolated from calf thymus glands in 1981 by Allan Goldstein at the George Washington University. It later drew attention when researchers noticed elevated levels in areas of active tissue repair — including the heart after myocardial injury.

Mechanism of Action

TB-500 binds actin, a key structural protein inside cells, and appears to influence how cells reorganize their internal skeleton to migrate. In cardiac injury models it has been observed to recruit progenitor cells and promote new capillary formation.

Studied In

  • Cardiac-repair and angiogenesis models
  • Soft-tissue and dermal wound closure
  • Inflammation and cell-migration signaling
  • Corneal and neural regeneration studies

Molecular Data

Formula:
C77H128N24O26
MW:
1888.06 g/mol
Length:
7 aa
CAS:
77591-33-4
Sequence:
LKKTETQ

Peer-Reviewed Citations

  1. Thymosin beta-4 promotes cardiac cell migration, survival and cardiac repair
    Bock-Marquette I, et al. · Nature · 2004 · PMID 15525938
  2. Thymosin beta-4 and its actin-binding activity in wound healing
    Goldstein AL, et al. · Ann N Y Acad Sci · 2005 · PMID 16174795
Growth & Performance· TH9507

Tesamorelin

The stabilized GHRH analog.

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In Plain English

Tesamorelin is a GHRH analog with a small chemical modification that makes it much more resistant to enzymatic breakdown. It's been extensively studied — including in large clinical trials — for its effects on visceral (deep abdominal) fat.

Discovery & Backstory

Developed by Theratechnologies in the 2000s. Landmark trials published in JAMA and NEJM examined its effects on visceral adipose tissue in specific clinical populations, making it one of the best-studied GHRH analogs in the peer-reviewed literature.

Mechanism of Action

Same pituitary GHRH-receptor activation as sermorelin, but with a hexenoic-acid N-terminal modification that resists degradation, producing a longer, more robust GH pulse profile.

Studied In

  • Visceral adipose-tissue reduction studies
  • Hepatic-fat and metabolic-marker research
  • IGF-1 and body-composition endpoints

Molecular Data

Formula:
C221H366N72O67S
MW:
5195.85 g/mol
Length:
44 aa
CAS:
218949-48-5

Peer-Reviewed Citations

  1. Effects of tesamorelin on visceral fat and liver fat in HIV-infected patients
    Stanley TL, et al. · JAMA · 2014 · PMID 25027142
Weight Management· GIP/GLP-1 Twincretin

Tirzepatide

The dual GIP + GLP-1 agonist.

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In Plain English

Tirzepatide is a single molecule engineered to activate two gut-hormone receptors at once — GIP and GLP-1 — instead of just one. In clinical research it has shown significantly greater effects on glucose regulation and body-composition markers than earlier single-target compounds.

Discovery & Backstory

Developed at Eli Lilly and introduced in the SURPASS and SURMOUNT trials published between 2021 and 2023. The 'twincretin' concept came from decades of endocrinology research showing that GIP and GLP-1 work synergistically in the healthy gut.

Mechanism of Action

Balanced agonism of GIP and GLP-1 receptors amplifies insulin release, suppresses glucagon, delays gastric emptying, and engages central appetite pathways. Dual activation appears to produce additive metabolic effects compared to single-receptor agonism.

Studied In

  • Dual-incretin receptor signaling
  • Glucose homeostasis and insulin sensitivity
  • Adipose-tissue and hepatic-fat research
  • Cardiovascular outcome studies

Molecular Data

Formula:
C225H348N48O68
MW:
4813.53 g/mol
Length:
39 aa
CAS:
2023788-19-2

Peer-Reviewed Citations

  1. Tirzepatide once weekly for the treatment of obesity
    Jastreboff AM, et al. · N Engl J Med · 2022 · PMID 35658024
  2. Dual GIP and GLP-1 receptor agonism in type 2 diabetes
    Frías JP, et al. · Lancet · 2021 · PMID 34186022

All content is provided for laboratory reference only. Citations are indexed in the U.S. National Library of Medicine. Nothing on this page constitutes medical advice, dosing guidance, or a claim of therapeutic effect in humans.

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