Peptide Wiki

Mechanism of Action

BPC-157 is a synthetic peptide derived from a protective protein found in human gastric juice. It promotes angiogenesis (new blood vessel formation) through upregulation of VEGF and the FAK-paxillin pathway. It also modulates the nitric oxide system and interacts with the dopaminergic system, contributing to its broad tissue-protective effects across muscle, tendon, ligament, and GI tissue.

Key Research Findings

• Accelerated healing of severed Achilles tendons in rat models, with restored mechanical properties within 72 hours (Staresinic et al., 2003)
• Demonstrated cytoprotective effects on gastric mucosa and accelerated healing of inflammatory bowel disease lesions in multiple rodent models (Sikiric et al., 1999)
• Promoted muscle healing after crush injuries with significant improvement in functional recovery compared to controls (Pevec et al., 2010)
• Counteracted NSAID-induced gastrointestinal damage in rats, maintaining mucosal integrity (Sikiric et al., 2006)
• Shown neuroprotective properties in dopaminergic system models, reversing damage from both agonists and antagonists (Sikiric et al., 2010)

Research Dosages

In published animal studies, typical dosages range from 10 mcg/kg to 50 mcg/kg administered intraperitoneally or subcutaneously. Most studies use daily administration over 7-14 day periods. Oral administration has also shown efficacy in GI-related models at similar dose ranges.

Related Compounds

TB-500 (often used in combination), GHK-Cu (complementary wound healing), KPV (anti-inflammatory synergy)

Mechanism of Action

TB-500 is the synthetic version of the naturally occurring Thymosin Beta-4 peptide. Its primary mechanism involves sequestering G-actin monomers, which promotes cell migration and differentiation during tissue repair. It upregulates actin production, enabling cells to move through damaged tissue more effectively. TB-500 also promotes angiogenesis and reduces inflammation by downregulating inflammatory cytokines.

Key Research Findings

• Accelerated dermal wound healing and hair growth in rodent models through enhanced cell migration (Philp et al., 2004)
• Reduced infarct size and improved cardiac function after myocardial infarction in mouse models (Bock-Marquette et al., 2004)
• Demonstrated anti-inflammatory effects by reducing levels of pro-inflammatory cytokines in corneal injury models (Sosne et al., 2007)
• Promoted neuronal survival and improved functional outcomes in traumatic brain injury models (Xiong et al., 2012)

Research Dosages

Animal studies typically use 1-6 mg/kg dosing, administered subcutaneously. Research protocols often involve an initial loading phase of higher doses followed by maintenance dosing over several weeks.

Related Compounds

BPC-157 (commonly stacked), GHK-Cu, Thymosin Alpha-1

Mechanism of Action

This blend combines two complementary repair peptides. BPC-157 acts primarily through VEGF-mediated angiogenesis and nitric oxide modulation, while TB-500 works through actin regulation and cell migration. Together, they address different phases of the healing cascade – BPC-157 focusing on vascular repair and GI protection, TB-500 on cellular mobility and inflammation reduction.

Key Research Findings

• Individual components have extensive independent research (see BPC-157 and TB-500 entries)
• Theoretical synergy based on complementary mechanisms – BPC-157 promotes blood vessel formation while TB-500 enhances cell migration to repair sites
• Both peptides independently show broad tissue-protective effects across multiple organ systems

Related Compounds

GHK-Cu, KPV, Thymosin Alpha-1

Mechanism of Action

GHK-Cu is a naturally occurring tripeptide that binds copper with high affinity. It modulates the activity of metalloproteinases (MMPs), promotes collagen synthesis, and stimulates glycosaminoglycan production. The copper ion is essential for numerous enzymatic processes including superoxide dismutase activity. GHK-Cu activates wound repair genes and suppresses genes associated with inflammation and tissue destruction.

Key Research Findings

• Stimulated collagen synthesis in human fibroblasts by 70% and glycosaminoglycan production by 56% (Maquart et al., 1999)
• Promoted wound contraction and increased angiogenesis in dermal wound models (Pickart, 2008)
• Gene expression studies showed upregulation of 1,584 genes and downregulation of 917 genes, with significant effects on DNA repair, antioxidant, and anti-inflammatory pathways (Campbell et al., 2012)
• Demonstrated hair growth-stimulating properties by enlarging hair follicle size in skin organ cultures (Pyo et al., 2007)

Research Dosages

Topical research applications typically use 1-3% solutions. Injectable research protocols vary from 50-200 mcg administered subcutaneously. Stability in solution is limited, so fresh preparation is recommended.

Related Compounds

BPC-157, Epithalon, Thymosin Alpha-1

Mechanism of Action

SS-31 selectively targets the inner mitochondrial membrane by binding to cardiolipin, a phospholipid critical for electron transport chain function. This interaction stabilizes cristae structure, optimizes electron transfer, and reduces reactive oxygen species (ROS) production at the source. Unlike conventional antioxidants that scavenge free radicals after formation, SS-31 prevents excessive ROS generation while maintaining physiological signaling.

Key Research Findings

• Concentrated over 1,000-fold within mitochondria compared to extracellular space (Zhao et al., 2004)
• Protected against ischemia-reperfusion injury in cardiac tissue by preserving mitochondrial function (Szeto, 2008)
• Improved skeletal muscle performance in aged mice by restoring mitochondrial energetics (Siegel et al., 2013)
• Currently in clinical trials for Barth syndrome, heart failure, and age-related mitochondrial dysfunction

Research Dosages

Animal studies typically use 0.1-3 mg/kg subcutaneously or intravenously. Clinical trials have explored doses ranging from 0.01 to 0.25 mg/kg/hour as continuous infusion.

Related Compounds

MOTS-c (mitochondrial peptide), NAD+ (mitochondrial support), 5-Amino-1MQ (metabolic)

Mechanism of Action

KPV is the C-terminal tripeptide fragment of alpha-melanocyte-stimulating hormone (alpha-MSH). It retains the anti-inflammatory properties of the parent hormone without its melanogenic effects. KPV enters cells and directly inhibits NF-kB activation by preventing its nuclear translocation. This blocks the transcription of pro-inflammatory cytokines including IL-1beta, IL-6, and TNF-alpha. It also interacts with inflammatory pathways independently of melanocortin receptors.

Key Research Findings

• Reduced inflammatory markers in colitis models by inhibiting NF-kB signaling (Kannengiesser et al., 2008)
• Demonstrated antimicrobial activity against Staphylococcus aureus and Candida albicans (Cutuli et al., 2000)
• Preserved anti-inflammatory activity through oral delivery in intestinal inflammation models (Dalmasso et al., 2008)
• Showed wound-healing properties in cutaneous models through reduced local inflammation (Brzoska et al., 2008)

Research Dosages

In animal studies, dosages of 10-200 mcg have been used via subcutaneous injection. Oral research applications have also demonstrated efficacy in GI inflammation models.

Related Compounds

BPC-157 (GI protection), Thymosin Alpha-1 (immune modulation), Selank (anti-inflammatory)

Mechanism of Action

Semaglutide mimics the incretin hormone GLP-1 with modifications that extend its half-life to approximately 7 days (native GLP-1 lasts about 2 minutes). It binds to GLP-1 receptors in the pancreas to stimulate glucose-dependent insulin secretion and suppress glucagon release. In the brain, it acts on hypothalamic appetite centers to reduce hunger and promote satiety. The C18 fatty acid chain enables albumin binding in plasma, protecting it from DPP-4 degradation.

Key Research Findings

• STEP 1 trial: 14.9% mean body weight reduction over 68 weeks at 2.4 mg weekly dose vs 2.4% for placebo (Wilding et al., NEJM, 2021)
• SUSTAIN-6: 26% reduction in major adverse cardiovascular events in type 2 diabetes patients (Marso et al., NEJM, 2016)
• SELECT trial: 20% reduction in cardiovascular events in overweight/obese patients without diabetes (Lincoff et al., NEJM, 2023)
• Demonstrated neuroprotective properties in Parkinson’s and Alzheimer’s disease models (Holscher, 2022)

Research Dosages

Clinical protocols use gradual dose escalation starting at 0.25 mg weekly, increasing monthly to a target of 1.0 mg (diabetes) or 2.4 mg (weight management). Animal research uses proportionally adjusted doses.

Related Compounds

Tirzepatide (dual agonist), Retatrutide (triple agonist), AOD-9604 (alternative metabolic peptide)

Mechanism of Action

Tirzepatide is the first dual GIP and GLP-1 receptor agonist. It activates both incretin receptor pathways simultaneously, producing additive effects on insulin secretion, appetite suppression, and metabolic regulation. The GIP component adds unique effects on fat metabolism and energy expenditure not achieved by GLP-1 alone. A C20 fatty acid side chain enables weekly dosing through extended albumin binding.

Key Research Findings

• SURMOUNT-1: 22.5% mean weight reduction at highest dose (15 mg) over 72 weeks vs 2.4% placebo (Jastreboff et al., NEJM, 2022)
• SURPASS trials: Superior HbA1c reduction compared to semaglutide 1 mg in type 2 diabetes (Frias et al., NEJM, 2021)
• SURMOUNT-2: 14.7% weight reduction in obese type 2 diabetes patients (Garvey et al., Lancet, 2023)
• Improved liver fat content by 8.09% vs placebo in NAFLD-related studies (Gastaldelli et al., 2022)

Research Dosages

Clinical dose escalation: 2.5 mg weekly for 4 weeks, then 5 mg, with optional increases to 10 mg and 15 mg at 4-week intervals.

Related Compounds

Semaglutide (GLP-1 only), Retatrutide (triple agonist), AOD-9604

Mechanism of Action

Retatrutide is the first triple agonist targeting GIP, GLP-1, and glucagon receptors simultaneously. The GLP-1 and GIP components suppress appetite and improve glucose handling, while the glucagon receptor activation increases energy expenditure through hepatic lipid oxidation and thermogenesis. This three-pronged approach produces the most aggressive weight reduction observed among incretin-based therapies in clinical trials to date.

Key Research Findings

• Phase 2 trial: 24.2% mean weight reduction at 12 mg dose over 48 weeks, the highest observed in any obesity drug trial (Jastreboff et al., NEJM, 2023)
• 58% of participants at the highest dose achieved 20% or greater body weight loss
• Significant improvements in metabolic biomarkers including triglycerides, HDL cholesterol, and liver enzymes
• Phase 3 trials currently underway for obesity, type 2 diabetes, and NASH

Research Dosages

Phase 2 protocol: dose escalation from 0.5 mg weekly to target doses of 1, 4, 8, or 12 mg over 24-48 weeks.

Related Compounds

Tirzepatide (dual agonist), Semaglutide (single agonist), AOD-9604

Mechanism of Action

AOD-9604 is a modified fragment of human growth hormone (amino acids 177-191) designed to retain the fat-reducing effects of GH without its growth-promoting or diabetogenic properties. It stimulates lipolysis (fat breakdown) and inhibits lipogenesis (fat formation) through interaction with beta-3 adrenergic receptors. Unlike full-length GH, AOD-9604 does not increase IGF-1 levels or affect blood glucose.

Key Research Findings

• Reduced body fat in obese Zucker rats without affecting IGF-1 levels or glucose tolerance (Ng et al., 2000)
• Phase 2b clinical trial showed significant fat mass reduction with oral dosing (Heffernan et al., 2011)
• Demonstrated cartilage repair properties in osteoarthritis models, leading to FDA GRAS classification for food use (Metabolic Pharmaceuticals)
• No antibody formation detected in human studies, indicating good immunological tolerance

Research Dosages

Animal studies use 250-500 mcg/kg. Human trials explored oral doses of 1 mg daily and subcutaneous doses of 250-500 mcg daily.

Related Compounds

CJC-1295 + Ipamorelin (GH axis), MOTS-c (metabolic), 5-Amino-1MQ (fat metabolism)

Mechanism of Action

5-Amino-1MQ selectively inhibits nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed in adipose tissue of obese individuals. NNMT degrades NAD+ and SAM (S-adenosylmethionine), both essential for energy metabolism. By blocking NNMT, 5-Amino-1MQ increases intracellular NAD+ and SAM levels, which activates Sirtuin 1 (SIRT1) signaling and boosts cellular energy expenditure. This shifts adipocytes from energy storage toward energy consumption.

Key Research Findings

• Reduced body weight by 7% in diet-induced obese mice over 11 days without affecting food intake (Neelakantan et al., 2018)
• Decreased fat cell size and lipid content in treated adipocyte cultures by over 50% (Neelakantan et al., 2018)
• Increased NAD+ content in treated cells, reversing the metabolic dysfunction associated with NNMT overexpression
• Did not cross the blood-brain barrier, limiting off-target central nervous system effects

Research Dosages

Animal studies use 10-20 mg/kg daily via intraperitoneal injection. Oral bioavailability is still under investigation.

Related Compounds

NAD+ (boosted by NNMT inhibition), AOD-9604, MOTS-c

Mechanism of Action

MOTS-c is encoded in the mitochondrial genome and acts as a mitochondrial-derived signaling peptide. It activates AMPK (AMP-activated protein kinase) – the master energy sensor of the cell – by inhibiting the folate cycle and de novo purine biosynthesis pathway. This triggers a cascade that enhances glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. MOTS-c also translocates to the nucleus during metabolic stress to regulate adaptive gene expression.

Key Research Findings

• Prevented age-dependent and high-fat-diet-induced insulin resistance in mice (Lee et al., Cell Metabolism, 2015)
• Improved exercise capacity and physical performance in aged mice (Reynolds et al., 2021)
• Endogenous MOTS-c levels decline with age and correlate with metabolic health markers (Kim et al., 2018)
• Nuclear translocation during metabolic stress regulates over 800 genes involved in cellular homeostasis (Kim et al., 2018)

Research Dosages

Mouse studies use 5-15 mg/kg daily via intraperitoneal injection. Human clinical trials are currently in progress at various dosing levels.

Related Compounds

SS-31 (mitochondrial targeting), NAD+ (energy metabolism), 5-Amino-1MQ (AMPK pathway overlap)

Mechanism of Action

CJC-1295 (no DAC) is a modified version of growth hormone-releasing hormone (GHRH) with four amino acid substitutions that protect it from enzymatic degradation. It binds to GHRH receptors on the anterior pituitary, stimulating the natural pulsatile release of growth hormone. Unlike the DAC (Drug Affinity Complex) version, the no-DAC variant produces acute GH pulses rather than sustained elevation, more closely mimicking natural physiology.

Key Research Findings

• Increased GH secretion 2-10 fold above baseline in human subjects without affecting the natural pulsatile pattern (Ionescu & Bhargava, 2011)
• Synergistic GH release when combined with GHRP-class peptides like Ipamorelin (Bowers et al., 2004)
• Did not significantly alter prolactin, cortisol, or FSH/LH levels at standard doses
• Half-life of approximately 30 minutes vs 7 minutes for native GHRH

Research Dosages

Research protocols typically use 100 mcg per administration, often combined with Ipamorelin at similar doses. Standard protocols involve 1-3 administrations daily, usually timed around sleep and fasting windows.

Related Compounds

Ipamorelin (commonly stacked GHRP), AOD-9604 (GH fragment)

Mechanism of Action

Ipamorelin is a selective growth hormone secretagogue that binds to the ghrelin/GHS receptor (GHSR) on pituitary somatotrophs. It triggers GH release through a pathway independent of GHRH, making it synergistic when combined with CJC-1295. Ipamorelin is considered the most selective GHRP because it stimulates GH release without significantly increasing cortisol, ACTH, or prolactin at effective doses – a key differentiator from older GHRPs like GHRP-6 and hexarelin.

Key Research Findings

• Dose-dependent GH release with minimal effect on ACTH, cortisol, and prolactin (Raun et al., 1998)
• Improved bone mineral content in ovariectomized rats, suggesting anti-osteoporotic properties (Svensson et al., 2000)
• No desensitization observed after repeated daily dosing over extended periods in animal studies
• Synergistic GH release when administered alongside GHRH analogues – combined output exceeds the sum of individual effects

Research Dosages

Research protocols use 100-300 mcg per administration via subcutaneous injection. Typically dosed 1-3 times daily, often paired with CJC-1295 (no DAC) at equimolar doses.

Related Compounds

CJC-1295 no DAC (standard combination), AOD-9604, DSIP (sleep/GH link)

Mechanism of Action

Semax is a synthetic analogue of ACTH(4-10) with an added Pro-Gly-Pro tail that protects against enzymatic degradation. It increases BDNF (brain-derived neurotrophic factor) expression in the hippocampus and cortex, promoting neuronal survival and synaptic plasticity. Semax also modulates serotonergic and dopaminergic systems, influences the expression of neurotrophins NGF and NT-3, and has immunomodulatory properties through effects on cytokine expression.

Key Research Findings

• Increased BDNF mRNA expression by 1.4-1.8 fold in rat hippocampus and cortex (Dolotov et al., 2006)
• Improved cognitive performance in attention and memory tasks in human subjects (Kaplan et al., 1996)
• Neuroprotective in ischemic stroke models, reducing infarct volume and improving neurological outcomes (Gusev et al., 2005)
• Approved in Russia and Ukraine for treatment of stroke, cognitive disorders, and peptic ulcers

Research Dosages

Intranasal dosing typically ranges from 100-600 mcg daily divided into 2-3 administrations. Standard clinical dose in Russia is 600 mcg/day intranasally.

Related Compounds

Selank (anxiolytic counterpart), Dihexa (cognitive), NAD+ (neuroprotection)

Mechanism of Action

Selank is a synthetic analogue of the immunomodulatory peptide tuftsin, extended with a Pro-Gly-Pro sequence for stability. It modulates the GABAergic system, increasing GABA-A receptor sensitivity without direct binding (unlike benzodiazepines). Selank also influences the balance of T-helper 1 and T-helper 2 cytokines, inhibits enkephalinase (preserving endogenous opioids), and increases BDNF expression. These combined effects produce anxiolytic and cognitive-enhancing properties without sedation or dependence.

Key Research Findings

• Reduced anxiety in generalized anxiety disorder comparable to medazepam (benzodiazepine) without sedation or cognitive impairment (Zozulya et al., 2008)
• Modulated expression of 36 genes related to GABAergic neurotransmission in hippocampal neurons (Volkova et al., 2016)
• Enhanced immune function through increased IL-6 expression and immunoglobulin production (Uchakina et al., 2008)
• Approved in Russia as an anxiolytic and nootropic medication since 2009

Research Dosages

Intranasal dosing of 250-750 mcg daily divided into 2-3 administrations. Russian clinical protocols typically use 300 mcg 3x daily.

Related Compounds

Semax (often paired), DSIP (sleep/anxiety), Thymosin Alpha-1 (immune link)

Mechanism of Action

Dihexa is a modified derivative of angiotensin IV that acts as a potent agonist of hepatocyte growth factor (HGF) and its receptor c-Met. This pathway is critical for synaptogenesis (new synapse formation) and neuronal connectivity. Dihexa has been described as approximately 10 million times more potent than BDNF at promoting new synapse formation. It crosses the blood-brain barrier and drives the formation of new dendritic spines and functional synaptic connections in the hippocampus.

Research integrity note: The 2014 Benoist et al. paper that established much of the HGF/c-Met mechanistic framework for Dihexa was retracted in April 2025 following concerns about image manipulation. While earlier studies (McCoy et al., 2013; Hay et al., 2019) documenting cognitive effects remain intact, the specific synaptogenic mechanism requires independent verification.

Key Research Findings

• Restored cognitive function in scopolamine-impaired rats at picomolar concentrations (McCoy et al., 2013)
• Increased dendritic spine density and synapse formation in hippocampal cultures (Benoist et al., 2014 — note: this paper was retracted in April 2025 due to image manipulation concerns; the HGF/c-Met mechanistic claims should be interpreted with caution pending independent replication)
• Effective via oral administration due to good blood-brain barrier penetration and metabolic stability
• Rescued age-related cognitive decline in aged rats across multiple memory paradigms (Hay et al., 2019)

Research Dosages

Animal studies use extremely low doses: 50 pmol/kg to 2 mg/kg depending on route (intracerebral vs oral). Oral studies in rats used approximately 0.5-2 mg/kg.

Related Compounds

Semax (BDNF pathway), Selank (cognitive), NAD+ (neuroprotection)

Mechanism of Action

DSIP was originally isolated from the blood of rabbits during induced sleep. It modulates sleep architecture by promoting delta wave (slow-wave) sleep through interactions with multiple neurotransmitter systems. DSIP influences GABA, glutamate, and serotonin signaling. It also acts as a stress-protective factor, normalizing cortisol and ACTH responses under stress, and appears to modulate endorphin and enkephalin systems. Its exact receptor target remains debated, but its effects on sleep staging are well-documented.

Key Research Findings

• Increased delta wave sleep percentage and reduced sleep latency in human insomnia studies (Schneider-Helmert & Schoenenberger, 1983)
• Normalized disturbed cortisol patterns and reduced stress hormone responses (Graf & Kastin, 1986)
• Demonstrated analgesic properties in chronic pain models, possibly through met-enkephalin modulation (Yehuda & Carasso, 1987)
• Anti-oxidant and free radical scavenging activity documented in vitro (Khvatova et al., 2003)

Research Dosages

Human studies used doses of 25-50 mcg/kg intravenously or subcutaneously, typically administered in the evening. Animal studies use similar weight-adjusted doses.

Related Compounds

Selank (GABA modulation), Ipamorelin (sleep-GH link), Epithalon (circadian rhythm)

Mechanism of Action

Epithalon is a synthetic version of the naturally occurring pineal gland peptide epithalamin. Its primary mechanism is the activation of telomerase, the enzyme responsible for maintaining telomere length during cell division. By reactivating telomerase in somatic cells, Epithalon delays the onset of replicative senescence. It also stimulates melatonin production from the pineal gland, regulates neuroendocrine function, normalizes circadian rhythms, and influences antioxidant enzyme expression.

Key Research Findings

• Activated telomerase and elongated telomeres in human somatic cells, extending replicative capacity by 33% (Khavinson et al., 2003)
• Increased lifespan by 10-15% in multiple rodent longevity studies (Anisimov et al., 2001, 2003)
• Restored evening melatonin levels in elderly primates to youthful baseline levels (Khavinson & Morozov, 2003)
• Reduced spontaneous tumor incidence in aging rodents by approximately 3.6-fold (Anisimov et al., 2002)

Research Dosages

Research protocols typically use 5-10 mg daily via subcutaneous injection for 10-20 day cycles, often repeated 2-3 times per year. Animal longevity studies used comparable weight-adjusted doses.

Related Compounds

NAD+ (aging pathway), GHK-Cu (gene expression), Thymosin Alpha-1 (immune aging)

Mechanism of Action

NAD+ is a critical coenzyme present in every living cell, essential for over 500 enzymatic reactions. It serves as an electron carrier in mitochondrial energy production (oxidative phosphorylation) and is consumed as a substrate by sirtuins (SIRT1-7), PARPs (DNA repair enzymes), and CD38 (immune signaling). NAD+ levels decline 40-50% with age, and this decline is linked to metabolic dysfunction, neurodegeneration, and accelerated aging. Direct supplementation or precursor-driven replenishment aims to restore youthful NAD+ levels.

Key Research Findings

• NAD+ levels decline approximately 50% between ages 40 and 60 in human tissue samples (Massudi et al., 2012)
• Restoring NAD+ levels improved mitochondrial function, insulin sensitivity, and exercise capacity in aged mice (Yoshino et al., Cell Metabolism, 2011)
• NMN (NAD+ precursor) supplementation improved vascular function and reduced arterial stiffness in aged mice (de Picciotto et al., Aging Cell, 2016)
• SIRT1 activation through elevated NAD+ improved DNA repair capacity and reduced age-related DNA damage (Li et al., Science, 2017)

Research Dosages

Intravenous research protocols typically use 250-750 mg per session. Subcutaneous protocols vary. Precursor studies (NMN/NR) use oral doses of 250-1000 mg daily.

Related Compounds

Epithalon (telomere pathway), 5-Amino-1MQ (NAD+ boosting via NNMT), MOTS-c (mitochondrial), SS-31

Mechanism of Action

Thymosin Alpha-1 is a thymic peptide that plays a central role in immune system maturation and regulation. It activates dendritic cells through Toll-like receptors (TLR2 and TLR9), enhances T-cell differentiation (both CD4+ and CD8+), and promotes NK cell activity. It increases the production of interferon-alpha and interferon-gamma while balancing Th1/Th2 immune responses. Unlike immunosuppressants, Ta1 modulates rather than suppresses, making it useful in both immunodeficiency and autoimmune contexts.

Key Research Findings

• Approved in over 35 countries for treatment of hepatitis B and C, with improved viral clearance rates (Garaci, 2007)
• Enhanced vaccine response in immunocompromised elderly patients, particularly influenza vaccination (Shen et al., 2007)
• Improved survival in sepsis patients by restoring immune competence in a multi-center clinical trial (Wu et al., Critical Care, 2013)
• Demonstrated anti-tumor immune enhancement when combined with checkpoint inhibitors in preclinical melanoma models (King & Bhatt, 2020)

Research Dosages

Standard clinical dose is 1.6 mg administered subcutaneously 2x weekly. Hepatitis protocols use 1.6 mg twice weekly for 6-12 months. Critical care studies used 1.6 mg daily for 7 days.

Related Compounds

TB-500 (Thymosin Beta-4 – same family), KPV (immune modulation), Selank (immune-cognitive)

Mechanism of Action

PT-141 (Bremelanotide) is a cyclic peptide derived from Melanotan II. It acts as a non-selective agonist at melanocortin receptors MC1R, MC3R, MC4R, and MC5R, with particular affinity for MC4R in the central nervous system. Unlike PDE5 inhibitors that act on vasculature, PT-141 works through the hypothalamic pathways that regulate arousal and desire. MC4R activation in the medial preoptic area initiates downstream dopaminergic signaling that mediates its effects.

Key Research Findings

• FDA-approved in 2019 (as Vyleesi) for hypoactive sexual desire disorder in premenopausal women (Kingsberg et al., Obstet Gynecol, 2019)
• Phase 3 trials showed statistically significant improvement in desire scores vs placebo (RECONNECT study)
• Effective in men with erectile dysfunction who did not respond to PDE5 inhibitors (Diamond et al., 2004)
• Most common side effect: transient nausea (~40%), typically resolving within hours

Research Dosages

FDA-approved dose is 1.75 mg subcutaneously as needed. Clinical studies tested doses from 0.3-4 mg. No more than one dose per 24 hours and no more than 8 doses per month is the clinical recommendation.

Related Compounds

Melanotan II (parent compound), KPV (melanocortin system)

Mechanism of Action

Melanotan II is a synthetic cyclic peptide analogue of alpha-melanocyte-stimulating hormone (alpha-MSH). It activates all five melanocortin receptor subtypes (MC1R-MC5R). MC1R activation stimulates melanogenesis in melanocytes, increasing eumelanin production and skin pigmentation. MC3R and MC4R activation affects appetite regulation and sexual function. The broad receptor activation profile accounts for its multiple physiological effects including tanning, appetite suppression, and libido modulation.

Key Research Findings

• Induced significant skin darkening in fair-skinned subjects after UV exposure, with protective increases in melanin density (Dorr et al., 2000)
• Demonstrated erectile effects in male subjects through MC4R-mediated central pathways (Wessells et al., 1998)
• Appetite-suppressing effects observed through MC4R activation in hypothalamic feeding centers (Fan et al., 1997)
• Derivative PT-141 isolated its sexual function effects and received FDA approval as Vyleesi

Research Dosages

Dermatological research used doses of 0.01-0.03 mg/kg subcutaneously. Typical research protocols involve an initial loading phase of daily administrations followed by maintenance dosing.

Related Compounds

PT-141 (Bremelanotide – derived from MT-II), KPV (alpha-MSH fragment)