Peptide Reference Library · Updated March 2026
The Clinical Peptide
Reference Library
Comprehensive, evidence-based profiles for every peptide in the LHP catalog. Each entry includes mechanism of action, primary clinical applications, evidence level, and peer-reviewed citations from PubMed and major journals. Designed for licensed medical professionals.
For Medical Professionals Only. This library is an educational resource for NPI-verified clinicians.
Evidence levels are reported honestly — preclinical data is noted as such and not extrapolated to clinical claims.
All compounds are available through LHP's licensed 503A compounding pharmacy partners with physician prescription.
This content does not constitute medical advice or a treatment protocol.
Anti-Aging, Longevity & Cellular Health
Epigenetic modulators, mitochondrial support, and cellular regeneration peptides
Epithalon
Epitalon · Tetrapeptide-7 · Ala-Glu-Asp-Gly
Telomere-lengthening tetrapeptide originally isolated from the pineal gland. One of the most extensively studied longevity peptides, with human clinical data.
Mechanism of Action
Epithalon is a synthetic tetrapeptide (Ala-Glu-Asp-Gly) derived from epithalamin, a natural polypeptide extracted from bovine pineal gland. Its primary mechanism involves activation of telomerase, the enzyme responsible for maintaining and elongating telomere length in somatic cells. It also modulates pineal gland function, normalizing melatonin secretion rhythms, and has demonstrated antioxidant properties and regulation of the hypothalamic-pituitary axis. Research by Khavinson et al. has shown Epithalon upregulates expression of telomerase reverse transcriptase (hTERT) in human somatic cells.
Primary Clinical Applications
Administration Routes
Subcutaneous injection
Intramuscular
Evidence Level
Human clinical data available. Russian longitudinal studies (Khavinson, St. Petersburg Institute of Bioregulation) demonstrated reduced mortality in elderly patients over 6–15 year follow-up periods. Additional human data on telomere length and melatonin regulation. Most long-term outcome data from Russian cohorts — independently replicated data is limited.
Key Clinical References
[1]Khavinson VKh et al. Peptide regulation of aging. Bull Exp Biol Med. 2003. — Longitudinal study demonstrating reduced cardiovascular mortality in elderly patients receiving epithalamin/epithalon. PubMed 14961131 ↗
[2]Khavinson V et al. Epithalon activates telomerase and reduces aging signs in senescent human mammary epithelial cells. Ann NY Acad Sci. 2002. PubMed 12428793 ↗
[3]Anisimov VN et al. Inhibitory effect of the peptide epitalon on the development of spontaneous mammary tumors in HER-2/neu transgenic mice. Int J Cancer. 2002. PubMed 12115782 ↗
Regulatory status: Not FDA-approved. Compounded by licensed 503A pharmacy with physician prescription. Available through LHP catalog. Most human research conducted in Russia; Western clinical trials are limited.
Available via LHP — 10mg ($65) · 50mg ($125)
MOTS-c
Mitochondrial ORF of the 12S rRNA type-c
Mitochondrially-encoded peptide regulating metabolic homeostasis, insulin sensitivity, and exercise capacity. Endogenous levels decline with age.
Mechanism of Action
MOTS-c is a 16-amino acid peptide encoded within the mitochondrial 12S ribosomal RNA. It translocates to the nucleus in response to metabolic stress, where it activates AMPK signaling, modulates the folate-methionine cycle, and promotes mitochondrial biogenesis. It has demonstrated regulation of glucose homeostasis, skeletal muscle insulin sensitivity, and fatty acid oxidation. Circulating MOTS-c levels are elevated with exercise and decline with aging, establishing it as an endogenous exercise-mimetic.
Primary Clinical Applications
Administration Routes
Subcutaneous injection
Evidence Level
Strong preclinical; limited human data. Multiple mouse models show potent metabolic effects. One human cross-sectional study (Lee et al., 2019) found serum MOTS-c inversely correlated with age and T2DM. Phase I safety data exists but large-scale RCTs are not yet complete.
Key References
[1]Lee C et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443–454. PubMed 25738459 ↗
[2]Reynolds JC et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12:470. PubMed 33469041 ↗
[3]Lee C et al. Circulating levels of mitochondrial-derived peptides MOTS-c and SHLP2 increase during caloric restriction. Aging (Albany NY). 2019;11(3):744–758. PubMed 30741635 ↗
Regulatory status: Not FDA-approved. Investigational compound. Available through LHP 503A compounding with physician Rx.
Available via LHP — 10mg ($59) · 40mg ($150)
SS-31 (Elamipretide)
Szeto-Schiller Peptide 31 · MTP-131 · Bendavia
Cardiolipin-targeting mitochondrial protective peptide. The most clinically advanced mitochondria-targeted peptide, with multiple Phase II trials in heart failure and aging.
Mechanism of Action
SS-31 is a tetrapeptide (D-Arg-dimethylTyr-Lys-Phe-NH2) that selectively concentrates in the inner mitochondrial membrane, where it binds cardiolipin — the signature phospholipid of this membrane. By stabilizing cardiolipin, SS-31 preserves the cristae architecture essential for electron transport chain function, reduces mitochondrial ROS production, prevents cytochrome c release, and maintains ATP synthesis efficiency. It has demonstrated efficacy in multiple models of mitochondrial dysfunction, including ischemia-reperfusion, heart failure, and skeletal muscle aging.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIV infusion (trials)
Evidence Level
Multiple Phase II human trials completed. SPARCL trial (HFpEF), MOTOR trial (aging skeletal muscle), MMTT study (mitochondrial myopathy). FDA Accelerated Approval granted for Barth syndrome in 2023 under brand name Stealth BioTherapeutics. Strongest clinical evidence base of any mitochondria-targeted peptide.
Key Clinical References
[1]Tung C et al. Elamipretide: A Review of Its Structure, Mechanism of Action, and Therapeutic Potential. Int J Mol Sci. 2025;26:944. PubMed 39940682 ↗
[2]Chatfield KC et al. Elamipretide (MTP-131) improves mitochondrial function and skeletal muscle performance in adults with biopsy-proven mitochondrial myopathy. CHEST. 2019;155(5):1140-1151. PubMed 30978285 ↗
[3]Szeto HH, Birk AV. Serendipitous Discovery of Mitochondria-Targeted Peptides (SS Peptides). AAPS J. 2014;16(6):1254-1260. PubMed 25216853 ↗
Regulatory status: FDA Accelerated Approval for Barth syndrome (Stealth BioTherapeutics). Off-label compounded form available for broader clinical use via 503A with physician Rx.
Available via LHP — 10mg ($55) · 50mg ($160)
NAD+
Nicotinamide Adenine Dinucleotide
Master coenzyme for cellular energy metabolism and sirtuin activation. IV/injectable NAD+ achieves rapid plasma repletion versus oral precursors.
Mechanism of Action
NAD+ is a coenzyme central to cellular redox reactions and energy metabolism, serving as electron carrier in the mitochondrial electron transport chain. It is also the substrate for sirtuin deacetylases (SIRT1-7), which regulate gene expression, DNA repair, and metabolic adaptation; and for PARP enzymes involved in DNA damage repair. Intracellular NAD+ declines approximately 50% between ages 40–60. Injectable NAD+ bypasses first-pass metabolism and oral bioavailability limitations, achieving plasma repletion within minutes.
Primary Clinical Applications
Administration Routes
IV infusionSubcutaneous injectionIntramuscular
Evidence Level
Multiple human trials; extensive mechanistic data. Human RCTs confirm IV NAD+ increases muscle NAD+ and improves insulin sensitivity. Clinical addiction recovery programs have used IV NAD+ infusions with published outcome data. Longevity applications primarily extrapolated from mechanistic and observational data.
Key References
[1]Martens CR et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat Commun. 2018;9:1286. PubMed 29599478 ↗
[2]Verdin E. NAD+ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208-1213. PubMed 26785494 ↗
Available via LHP — 500mg ($70) · 1000mg ($110)
FOXO4-DRI
FOXO4-p53 interfering peptide · Senolytic peptide
D-retro-inverso peptide that disrupts the FOXO4-p53 interaction in senescent cells, triggering selective apoptosis. One of the most targeted senolytic approaches in current research.
Mechanism of Action
Senescent cells persist by having FOXO4 sequester p53 in the nucleus, preventing apoptosis. FOXO4-DRI is a D-amino acid retro-inverso peptide (protease-resistant) that competitively disrupts the FOXO4-p53 interaction, freeing p53 to trigger apoptosis selectively in senescent cells. Non-senescent cells are largely unaffected. The D-retro-inverso design gives it high metabolic stability compared to standard L-amino acid peptides.
Primary Research Applications
Administration Routes
Subcutaneous injection
Evidence Level
Preclinical only — no published human trials. Seminal Nature Medicine paper (Baar et al., 2017) showed dramatic restoration of physical fitness and organ function in fast-aging and naturally aged mice. No human dose-finding, safety, or efficacy data published. Highly experimental — clinical use requires thorough informed consent.
Key Reference
[1]Baar MP et al. Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging. Cell. 2017;169(1):132-147. PubMed 28340339 ↗
Highly experimental: No human safety or efficacy data published. Physician judgment and documented informed consent are mandatory. This is among the most investigational compounds in the LHP catalog.
Available via LHP — 10mg ($180)
L-Glutathione (Reduced)
GSH · γ-Glu-Cys-Gly · Master antioxidant tripeptide
The cell's primary endogenous antioxidant. Injectable GSH bypasses poor oral bioavailability, achieving plasma levels 10-30x higher than oral supplementation. Declines with age and chronic illness.
Mechanism of Action
Glutathione (Glu-Cys-Gly) is the most abundant intracellular antioxidant. Its reduced thiol (-SH) form is biologically active. Core functions: direct ROS scavenging; regeneration of vitamins C and E from their oxidized forms; hepatic detoxification via glutathione-S-transferase conjugation of xenobiotics and heavy metals; DNA repair support; immune modulation (T-cell proliferation, NK cell activity). IV/injectable route achieves 10-30x the plasma concentrations of oral supplementation, which is largely degraded in the GI tract before absorption.
Primary Clinical Applications
Administration Routes
IV infusionSubcutaneous injectionIntramuscular
Evidence Level
Human clinical data across multiple indications. RCTs confirm melanin reduction and skin brightening. Parkinson's neuroprotection RCTs (Holmay et al.). Hepatic protection in alcoholic and non-alcoholic liver disease. Athletic recovery pilot RCTs. Standard of care in some integrative oncology settings.
Key References
[1]Pizzorno J. Glutathione! Integr Med (Encinitas). 2014;13(1):8-12. PMC4684116 ↗
Available via LHP — 600mg ($85)
Growth Hormone Secretagogues (GHS)
GHRH analogs and GHRPs that stimulate physiological, pulsatile GH release
Sermorelin
GRF 1-29 · Geref (discontinued) · GHRH analog
Synthetic 29-amino acid analog of endogenous GHRH. Previously FDA-approved for GH deficiency in children; compounded form widely used in adult longevity medicine. Stimulates physiological pulsatile GH release.
Mechanism of Action
Sermorelin is the N-terminal 29-amino acid fragment of endogenous human GHRH, retaining full biological activity. It binds the GHRH receptor on pituitary somatotrophs, activating cAMP signaling to stimulate GH gene transcription and secretion. Unlike exogenous recombinant GH, sermorelin preserves the physiological pulsatile pattern of GH release and remains subject to negative feedback via somatostatin, making sustained supraphysiological GH levels pharmacologically difficult to achieve. Half-life of 11–12 minutes (SQ). Stimulates endogenous IGF-1 production downstream.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionTypically bedtime dosing
Evidence Level
Strong human evidence. FDA-approved 1990 (diagnostic), 1997 (pediatric GH deficiency treatment). Withdrawn 2008 for commercial (not safety) reasons — FDA has confirmed it was not withdrawn for safety or efficacy concerns. Multiple RCTs confirm GH and IGF-1 elevation in adults; sleep and cognitive benefits in randomized trials by Vitiello et al. and Merriam et al.
Key Clinical References
[1]Walker RF. Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin Interv Aging. 2006;1(4):307-308. PMC2699646 ↗
[2]Vitiello MV et al. Growth hormone-releasing hormone improves the cognition of healthy older adults. Neurobiol Aging. 2006;27(2):318-323. PubMed 16399215 ↗
[3]Sinha DK et al. Beyond the androgen receptor: growth hormone secretagogues in hypogonadal males. Transl Androl Urol. 2020;9:S149-S159. PMC7108996 ↗
[4]Ishida J et al. Growth hormone secretagogues: history, mechanism of action, and clinical development. JCSM Rapid Commun. 2020;3:25-37. PubMed 32051890 ↗
Regulatory status: Previously FDA-approved (Geref); withdrawn for commercial reasons (not safety). FDA confirmed it may be legally prescribed and compounded. Available via 503A pharmacy with physician Rx. Off-label prescribing is not federally prohibited.
Available via LHP — 5mg ($58) · 10mg ($105)
Tesamorelin
Egrifta · TH9507 · trans-3-hexenoic acid-GHRH(1-44)
FDA-approved GHRH analog with enhanced half-life. Only GH secretagogue with active US marketing authorization. Strongest evidence base in the GHS class.
Mechanism of Action
Tesamorelin is the full 44-amino acid GHRH sequence modified with a trans-3-hexenoic acid group at the N-terminus, which confers resistance to dipeptidyl peptidase IV (DPP-IV) degradation and extends half-life compared to sermorelin. It binds the GHRH receptor with high affinity, producing a stronger and more sustained pulse of pituitary GH secretion. Still subject to somatostatin feedback — physiological pulsatility maintained. Downstream effects: increased serum GH, elevated IGF-1, preferential reduction of visceral adipose tissue (VAT).
Primary Clinical Applications
Administration Routes
Subcutaneous injection (daily)
Evidence Level
FDA-approved (Phase III RCT data). Egrifta approval based on two Phase III RCTs showing significant VAT reduction vs. placebo in HIV lipodystrophy. Additional RCTs in metabolic syndrome and early Alzheimer's disease (Baker et al., JAMA Neurol 2021 — significant cognitive and metabolic effects). Tesamorelin combination protocols with ipamorelin widely used clinically.
Key Clinical References
[1]Falutz J et al. Metabolic effects of a growth hormone–releasing factor in patients with HIV. N Engl J Med. 2007;357(23):2359-2370. PubMed 18057339 ↗
[2]Baker LD et al. Effects of growth hormone–releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults. JAMA Neurol. 2021;78(4):452-460. PubMed 33565580 ↗
Regulatory status: FDA-approved under brand name Egrifta/Egrifta WR for HIV-associated lipodystrophy. Off-label compounded use for metabolic/longevity applications via 503A pharmacy with physician Rx.
Available via LHP — 5mg ($100) · 10mg ($160) · Blends with Ipamorelin available
Ipamorelin
NNC 26-0161 · Selective GHRP
Selective pentapeptide GHRP with minimal effect on cortisol and prolactin. Preferred combination partner with GHRH analogs for 2–4× synergistic GH release amplification.
Mechanism of Action
Ipamorelin is a synthetic pentapeptide that acts as a selective agonist of the ghrelin/GHS-R1a receptor on pituitary somatotrophs and hypothalamic neurons. Unlike GHRP-2 and GHRP-6, ipamorelin demonstrates high selectivity for GH release with minimal stimulation of cortisol, ACTH, or prolactin — making it the cleanest GHRP from an endocrine side-effect profile perspective. When combined with a GHRH analog (sermorelin or tesamorelin), the two receptor pathways act synergistically to produce 2–4× greater GH release than either compound alone.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionUsually with GHRH analog (2x blend)
Evidence Level
Phase II clinical trials completed; not FDA-approved. Ipamorelin advanced to Phase II trials for postoperative ileus (Helsinn Healthcare). GH-stimulating properties confirmed in human volunteers. Clinical protocols widely used in anti-aging medicine based on pharmacodynamic and safety data.
Key References
[1]Raun K et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. PubMed 9849822 ↗
[2]Sinha DK et al. Beyond the androgen receptor: growth hormone secretagogues in hypogonadal males. Transl Androl Urol. 2020;9:S149-S159. PMC7108996 ↗
Available via LHP — 5mg ($55) · 10mg ($75) · Blends with CJC-1295 and Tesamorelin available
CJC-1295
CJC-1295 with DAC (long-acting) · CJC-1295 without DAC (MOD-GRF 1-29)
Modified GHRH analog available in two forms: with Drug Affinity Complex (DAC) for extended half-life enabling weekly dosing, and without DAC (MOD-GRF 1-29) for pulsatile daily dosing. Commonly combined with ipamorelin for synergistic GH release.
Mechanism of Action — DAC vs. No DAC
Without DAC (MOD-GRF 1-29): Modified sermorelin analog with 4 amino acid substitutions increasing resistance to DPP-IV degradation. Half-life ~30 minutes. Produces discrete GH pulses ideal for bedtime dosing with ipamorelin — mimics physiological pulsatility. Preferred for protocols prioritizing natural GH dynamics.
With DAC: Same peptide backbone conjugated to a lysine-drug affinity complex that binds serum albumin, extending half-life to ~8 days. Enables once-weekly dosing. Sustains elevated GH/IGF-1 levels more continuously — may partially blunt natural pulsatility, which is a tradeoff for convenience.
With DAC: Same peptide backbone conjugated to a lysine-drug affinity complex that binds serum albumin, extending half-life to ~8 days. Enables once-weekly dosing. Sustains elevated GH/IGF-1 levels more continuously — may partially blunt natural pulsatility, which is a tradeoff for convenience.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionNo-DAC: daily (bedtime)With DAC: 1-2x/week
Evidence Level
Phase I/II data (CJC-1295 with DAC); no FDA approval. Teichman et al. Phase II RCT (2006) demonstrated significant GH and IGF-1 elevation with once-weekly CJC-1295 DAC. No-DAC form studied primarily in the context of combination protocols. Not FDA-approved; widely used in clinical longevity practice.
Key Reference
[1]Teichman SL et al. Prolonged Stimulation of Growth Hormone (GH) and Insulin-Like Growth Factor I Secretion by CJC-1295, a Long-Acting Analog of GH-Releasing Hormone, in Healthy Adults. J Clin Endocrinol Metab. 2006;91(3):799-805. PubMed 16352683 ↗
Available via LHP — CJC Without DAC 5mg ($55) · 10mg ($88) · With DAC 5mg ($85) · 2x Blend with Ipamorelin ($105)
GHRP-2
Pralmorelin · KP-102 · Growth Hormone Releasing Peptide-2
Potent synthetic hexapeptide GHRP. FDA-approved in Japan (Kaken) as a GH stimulation test agent. Second most selective GHRP after ipamorelin — mild cortisol/prolactin effect. Produces 47-fold increase in pulsatile GH when combined with GHRH.
Mechanism of Action
GHRP-2 (Pralmorelin) is a synthetic hexapeptide agonist of the ghrelin/GHS-R1a receptor. It stimulates GH release from the anterior pituitary via phospholipase C and intracellular calcium mobilization — distinct from the cAMP pathway used by GHRH analogs. When combined with GHRH, the dual-pathway stimulation produces synergistic GH release: 47-fold increase in pulsatile GH secretion versus GHRH alone (20-fold). GHRP-2 produces modest elevations in cortisol and prolactin (less than GHRP-6); significant GH release without desensitization at clinical doses.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIV (diagnostic use)
Evidence Level
Approved in Japan (Kaken); extensive human data. FDA-approved in Japan under brand GHRP Kaken 100 for GH deficiency diagnosis. Multiple human pharmacodynamic studies confirming GH and IGF-1 elevation. Sinha et al. (2020) retrospective review in hypogonadal men demonstrated significant IGF-1 increase. Synergistic data with sermorelin/GHRH well-documented.
Key Reference
[1]Sinha DK et al. Beyond the androgen receptor: growth hormone secretagogues in hypogonadal males. Transl Androl Urol. 2020;9:S149-S159. PMC7108996 ↗
Available via LHP — 5mg ($50) · 10mg ($80)
GHRP-6
Growth Hormone Releasing Peptide-6 · Hexarelin analog
First-generation synthetic GHRP. Strongest GH-stimulating effect of the GHRP class, with notable appetite stimulation via ghrelin pathway activation. Useful when appetite promotion is a clinical goal alongside GH optimization.
Mechanism of Action
GHRP-6 is a first-generation hexapeptide GHS-R1a agonist with the strongest GH-stimulating activity of the GHRP class but also the broadest receptor activity. In addition to GHS-R1a, it activates ghrelin orexigenic pathways producing significant appetite stimulation and hunger — a key distinguishing feature from ipamorelin and GHRP-2. Also stimulates cortisol and prolactin more than newer-generation GHRPs. The appetite effect is both a side effect and a clinical feature: useful in cachexia, anorexia, or patients requiring weight gain. Produces robust GH release, especially in combination with GHRH analogs.
Primary Clinical Applications
Administration Routes
Subcutaneous injection
Evidence Level
Human pharmacodynamic data; not FDA-approved. Multiple human studies confirm robust GH and IGF-1 elevation. Human cardioprotection data exists (reduces ischemia-reperfusion injury in clinical settings). Appetite stimulation confirmed in human volunteers. Note: the strong appetite stimulation makes it less suitable for patients using GHS for body recomposition or fat loss goals — ipamorelin or GHRP-2 are preferred in those cases.
Available via LHP — 5mg ($60) · 10mg ($100)
Tissue Repair & Regenerative Peptides
Gastric-derived, thymic, and synthetic peptides for musculoskeletal and systemic tissue healing
BPC-157
Body Protective Compound-157 · Gastric Pentadecapeptide · PL-14736
15-amino acid peptide derived from human gastric juice with extensive preclinical regenerative data across tendon, ligament, muscle, bone, and GI tissue. High clinical interest; limited human RCT data.
Mechanism of Action
BPC-157 is a synthetic pentadecapeptide (GEPPPGKPADDAGLV) isolated from human gastric juice. Its regenerative effects operate through several interconnected pathways:
VEGFR2 activation promoting angiogenesis; Akt-eNOS axis driving nitric oxide synthesis for endothelial repair and vasodilation; FAK/Paxillin signaling enhancing cell adhesion and fibroblast migration; ERK1/2 pathway stimulating endothelial proliferation and vascular tube formation; NO-dependent cytoprotection reducing free radical damage. Additionally modulates growth hormone receptor expression at the peripheral level, potentially amplifying local GH effects at injury sites.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIntramuscularOral (GI applications)
Evidence Level
Strong preclinical; limited human RCT data. Systematic reviews (Vasireddi et al., Orthop J Sports Med 2025; McGuire et al., Curr Sports Med Rep 2025) covering 36–39 studies confirm robust preclinical regenerative effects across musculoskeletal models. Three published human studies exist — two open-label trials (knee pain, interstitial cystitis) and one Phase I safety study (Lee & Burgess 2025, IV infusion up to 20mg, no adverse events). FDA designated Category 2 bulk drug substance in 2023; no human RCTs completed. Clinical use is investigational.
Key References (2024–2025)
[1]Vasireddi N et al. Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. Orthop J Sports Med. 2025. PMC12313605 ↗
[2]McGuire F et al. Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing. Curr Sports Med Rep. 2025. PMC12446177 ↗
[3]Seiwerth S et al. BPC 157 and Wound Healing. Front Pharmacol. 2021. PMC8275860 ↗
[4]Khatri M et al. Injectable Therapeutic Peptides in Sports Medicine. Arthroscopy. 2024. Arthroscopy J. 2024 ↗
Regulatory status: FDA Category 2 bulk drug substance (2023) — cannot be compounded by 503B outsourcing facilities for commercial distribution, but can be prescribed and compounded 503A with physician Rx. WADA removed from banned list (previously listed 2022). Clinical use should be considered investigational pending human RCT data.
Available via LHP — 5mg ($55) · 10mg ($100) · "Wolverine" & "Glow" blends with TB500 & GHK-Cu
TB-500 (Thymosin Beta-4 Fragment)
Thymosin B4 Acetate · Tβ4 (1-44 fragment) · TB-4
Synthetic fragment of the endogenous actin-sequestering protein thymosin beta-4. Upregulates actin in wounded cells, promotes angiogenesis, and reduces inflammation. Widely combined with BPC-157.
Mechanism of Action
Thymosin Beta-4 is an endogenous 43-amino acid peptide abundantly expressed in platelets, macrophages, and wound fluid. TB-500 is the synthetic analog targeting its primary healing sequence. Mechanism involves: actin sequestration and polymerization facilitating cell migration to wound sites; upregulation of anti-apoptotic proteins (e.g., Ku80); VEGF stimulation promoting neovascularization; NF-κB inhibition reducing inflammatory cytokines; stem cell activation in cardiac tissue. Identified as an endogenous "exerkine" — exercise increases circulating Tβ4 levels in humans.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIntramuscular
Evidence Level
Phase II human trials completed for cardiac and dry eye applications. RegeneRx Biopharmaceuticals advanced Tβ4 to Phase II trials for anterior sternal wound healing, dry eye (RGN-259 — Phase III), and cardiac repair post-MI. Identified as human exerkine by Gonzalez-Franquesa et al. (2021). Musculoskeletal applications are primarily extrapolated from preclinical data.
Key References
[1]Gonzalez-Franquesa A et al. Discovery of thymosin β4 as a human exerkine and growth factor. Am J Physiol Cell Physiol. 2021;321:C770-C778. PubMed 34346766 ↗
[2]Goldstein AL et al. Thymosin β4 is an actin-sequestering protein important in regulation of cell shape and migration. Trends Cell Biol. 2012. PubMed 22498187 ↗
Regulatory status: Not FDA-approved for systemic use. RGN-259 (eye drop formulation) in Phase III for dry eye. Compounded systemic form available via 503A with physician Rx.
Available via LHP — 2mg ($50) · 5mg ($58) · 10mg ($100) · "Wolverine" blend with BPC-157
GHK-Cu
Glycyl-L-Histidyl-L-Lysine-Copper · Copper Tripeptide · TriHex
Naturally occurring human plasma tripeptide that complexes with copper(II). Declines from ~200 ng/mL at age 20 to ~80 ng/mL at age 60. Over 40 years of research confirm skin regeneration, wound healing, and broad gene regulatory effects.
Mechanism of Action
GHK is a tripeptide (Gly-His-Lys) with very high copper(II) affinity, forming the GHK-Cu complex. It is cleaved from collagen's alpha-2(I) chain during extracellular matrix damage, functioning as a tissue-damage signal. Mechanisms include: stimulation of collagen, elastin, and GAG synthesis in dermal fibroblasts; MMP/TIMP modulation (bidirectional, dose-dependent) for balanced matrix remodeling; VEGF/bFGF upregulation in irradiated fibroblasts; macrophage and capillary cell chemotaxis; and broad gene regulatory effects — Broad Institute CMap analysis shows GHK modulates 31.2% of human genes by ≥50%, with particular effects on DNA repair, antioxidant, and anti-inflammatory pathways.
Primary Clinical Applications
Administration Routes
Topical (primary)Subcutaneous injection
Evidence Level
Multiple human clinical trials. RCT in 40 women (aged 40–65) over 8 weeks showed GHK-Cu outperformed Matrixyl 3000 on collagen/elastin production. 71-woman 12-week trial confirmed improved skin density, thickness, and wrinkle reduction. 1999 human biopsy study found GHK-Cu increased collagen in 70% of subjects — outperforming vitamin C and retinoic acid. Post-laser RCT (facial resurfacing) showed higher patient satisfaction and perceptible wrinkle improvement.
Key References
[1]Pickart L, Margolina A. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. Int J Mol Sci. 2018;19(7):1987. PMC6073405 ↗
[2]Pickart L, Vasquez-Soltero JM, Margolina A. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. Biomed Res Int. 2015. PMC4508379 ↗
[3]Badenhorst T et al. Effects of GHK-Cu on MMP and TIMP Expression, Collagen and Elastin Production and Facial Wrinkle Parameters. J Aging Sci. 2016. RCT in 40 women. Walsh Medical ↗
Available via LHP — 50mg ($90) · 100mg ($150) · "Glow" & "Klow" blends with BPC-157 & TB500
GLP-1 / Incretin & Metabolic Peptides
Compounded receptor agonists and next-generation metabolic modulators
Semaglutide
Ozempic (T2DM) · Wegovy (obesity) · GLP-1 receptor agonist
FDA-approved GLP-1 receptor agonist. Most prescribed weight management medication in history. Compounded semaglutide extends access at fraction of branded cost under physician supervision.
Mechanism of Action
Semaglutide is a 94% homologous GLP-1 analog modified with a C18 fatty di-acid chain enabling albumin binding and extending half-life to ~168 hours (weekly dosing). Mechanism: GLP-1 receptor agonism in pancreatic beta cells → increased glucose-dependent insulin secretion; central hypothalamic signaling reducing appetite and caloric intake via arcuate nucleus GLP-1 receptors; gastric emptying delay extending satiety. Branded Ozempic/Wegovy use semaglutide base. Compounded forms may use semaglutide sodium or acetate salt forms — physicians should confirm molecular form with their compounding pharmacy.
Primary Clinical Applications
Administration Routes
Subcutaneous injection (weekly)
Evidence Level
Phase III FDA-approved (extensive RCT database). SUSTAIN series (T2DM), STEP series (obesity) — ~15% average body weight reduction at 68 weeks. SELECT trial (2023): 20% reduction in major cardiovascular events in non-diabetic obese adults. Compounded semaglutide carries the same mechanism — evidence for efficacy extrapolated from branded trials; specific safety data for salt-form compounded versions is limited.
Landmark Trials
[1]Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). N Engl J Med. 2021;384:989-1002. PubMed 33567185 ↗
[2]Lincoff AM et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes (SELECT). N Engl J Med. 2023;389:2221-2232. PubMed 37952130 ↗
Important note on compounded semaglutide: FDA-approved brands use semaglutide base. Compounded forms may use acetate or sodium salt — chemically distinct. Compounding is legal via 503A with physician Rx. The FDA removed semaglutide from the drug shortage list in 2025; confirm current 503A/503B compliance status with your LHP account manager.
Available via LHP — 5mg–60mg · Semaglutide + BPC blends available
Tirzepatide
Mounjaro (T2DM) · Zepbound (obesity) · GLP-1/GIP dual agonist
Dual GLP-1 and GIP receptor co-agonist (twincretin). Outperforms semaglutide in head-to-head trials. Highest weight-loss efficacy of any approved metabolic agent to date (~20–22% at 72 weeks).
Mechanism of Action
Tirzepatide is a 39-amino acid synthetic peptide with dual agonism at GLP-1R and GIPR. GIP receptor co-activation amplifies insulin secretion in a glucose-dependent manner, reduces glucagon, enhances fat oxidation via adipocyte GIPR signaling, and may contribute to reduced nausea compared to GLP-1 monotherapy. The dual mechanism produces additive-to-synergistic metabolic effects including superior insulin sensitivity, greater weight loss, and improved lipid profiles versus semaglutide. Half-life ~5 days enables weekly dosing.
Primary Clinical Applications
Administration Routes
Subcutaneous injection (weekly)
Evidence Level
Phase III FDA-approved; SURMOUNT series. SURMOUNT-1 (72 weeks): 20.9% average weight loss vs 3.1% placebo — largest approved weight-loss efficacy of any drug class. SURPASS CVOT (cardiovascular outcomes): significant reductions in MACE. FDA approved for obstructive sleep apnea (2024). Compounding regulatory note: 503B bulk tirzepatide compounding restricted per March 2025 federal court ruling — 503A patient-specific remains legal.
Landmark Trials
[1]Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity (SURMOUNT-1). N Engl J Med. 2022;387:205-216. PubMed 35658024 ↗
[2]Ludvik B et al. Once-weekly tirzepatide versus once-daily insulin degludec (SURPASS-3). Lancet. 2021;398:583-598. PubMed 34370985 ↗
Compounding regulatory update (March 2025): Federal court denied OFA's injunction — 503B outsourcing facilities must cease bulk tirzepatide compounding. LHP uses 503A patient-specific compounding with physician Rx, which remains fully legal and explicitly preserved by the regulatory framework. Confirm current supply status with LHP.
Available via LHP — 10mg–100mg · Tirzepatide + BPC blends available
Retatrutide
LY3437943 · GLP-1/GIP/Glucagon triple agonist · "Trireceptor agonist"
Next-generation triple agonist (GLP-1R + GIPR + GCGR). Phase II data: 17.5% weight loss at 24 weeks — the highest published weight-loss efficacy of any peptide in clinical trials. No branded product yet exists.
Mechanism of Action
Retatrutide is a once-weekly injectable peptide with balanced triple agonism at GLP-1R, GIPR, and GCGR. The addition of glucagon receptor co-activation to the GLP-1/GIP dual mechanism drives hepatic glucose production reduction, enhanced thermogenesis and energy expenditure (GCGR effect), and additional lipolysis in white adipose tissue. This triple mechanism theoretically addresses metabolic syndrome more comprehensively than dual agonists. Phase II data published in NEJM (2023) showed dose-dependent weight loss up to 17.5% at 24 weeks in obese adults without diabetes.
Primary Clinical Applications
Administration Routes
Subcutaneous injection (weekly)
Evidence Level
Phase II data only — no branded product approved. Jastreboff et al., NEJM 2023: Phase II RCT in 338 obese adults, doses up to 12mg weekly, 17.5% body weight reduction at 24 weeks (highest published weight-loss efficacy). Phase III trials (TRIUMPH series) ongoing. Compounded retatrutide is available now through LHP 503A — branded product does not yet exist.
Key Reference
[1]Jastreboff AM et al. Triple–Hormone-Receptor Agonist Retatrutide for Obesity — A Phase 2 Trial. N Engl J Med. 2023;389:514-526. PubMed 37366315 ↗
Regulatory status: Phase III trials ongoing (Eli Lilly). No branded product exists. Compounded form available via LHP 503A with physician Rx — this is the only way to clinically access retatrutide at present.
Available via LHP — 10mg ($140) through 60mg ($490) · Cagrilintide + Semaglutide combo available
Immune & Anti-Inflammatory Peptides
Thymic peptides and erythropoietin-derived immune modulators
Thymosin Alpha-1
Tα1 · Thymalfasin · Zadaxin
FDA-approved thymic peptide immune modulator (Zadaxin — international approvals). Approved in 35+ countries for hepatitis B/C, cancer adjunct, and sepsis. Extensive human clinical data.
Mechanism of Action
Thymosin Alpha-1 is a 28-amino acid peptide naturally secreted by thymic epithelial cells. Its immune modulatory effects operate through: T-cell receptor upregulation and enhancement of T-helper cell differentiation; NK cell and dendritic cell activation; Toll-like receptor (TLR) signaling modulation normalizing innate immune responses; cytokine regulation (increases IL-2, IFN-γ; reduces excessive pro-inflammatory cytokines). It acts as both an immune stimulant in immunodeficiency states and an immune regulator in hyperinflammatory states — a bidirectional modulator.
Primary Clinical Applications
Administration Routes
Subcutaneous injection
Evidence Level
Extensive human clinical data. Approved in 35+ countries. Marketed as Zadaxin (SciClone Pharmaceuticals) — approved for HBV, HCV, and as cancer adjunct. Multiple RCTs for hepatitis, sepsis adjunct therapy, and immune reconstitution. Not FDA-approved in the US; available via 503A compounding. Phase studies in COVID-19 showed significant reductions in mortality in severe cases (Zhang et al., 2020).
Key References
[1]Shrivastava P et al. Thymosin alpha 1: past, present and future. Expert Opin Biol Ther. 2010;10(7):1065-1078. PubMed 20560793 ↗
[2]Zhang Y et al. Thymosin alpha-1 reduces mortality of severe COVID-19 patients. Signal Transduct Target Ther. 2020;5:129. PubMed 32694598 ↗
Regulatory note: Approved (Zadaxin) in 35+ countries for hepatitis B, hepatitis C, and oncology adjunct use. Not FDA-approved in the US — available via 503A compounding with physician Rx. The FDA issued a warning letter to Paradigm Peptides (2020) for marketing Tα1 as a COVID-19 treatment without authorization — LHP's physician-supervised prescribing model is the compliant pathway.
Available via LHP — 2mg ($50) · 5mg ($65) · 10mg ($100)
Ara-290
Cibinetide · ERB-peptide · Innate Repair Receptor agonist
11-amino acid cyclic peptide derived from the helix B surface of erythropoietin (EPO). Binds the innate repair receptor (IRR) — a tissue-protective EPO receptor complex — without stimulating red blood cell production. Phase II trials in diabetic neuropathy and sarcoidosis.
Mechanism of Action
EPO has two receptor systems: the classical EPO-R homodimer (hematopoiesis) and the heterodimeric Innate Repair Receptor (IRR) consisting of EPO-R and the common beta-chain (βc/CD131), which mediates tissue protection. Ara-290 selectively binds the IRR without activating EPO-R, thus providing tissue-protective effects without erythropoietic risk (thrombosis, polycythemia). IRR activation reduces inflammatory cytokine production (TNF-α, IL-6, IL-1β), promotes peripheral nerve repair, reduces neuropathic pain signaling, and activates tissue repair pathways in multiple organ systems.
Primary Clinical Applications
Administration Routes
Subcutaneous injection
Evidence Level
Phase II RCTs completed — strong signal. Brines et al. RCT in diabetic neuropathy: significant improvement in corneal nerve fiber density, thermal detection thresholds, and neuropathic symptoms vs. placebo. Heij et al. Phase II in sarcoidosis-related small fiber neuropathy: significant reduction in neuropathic pain and improved corneal nerve fiber length. Safety profile excellent — no EPO-related effects.
Key References
[1]Brines M et al. Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin. Proc Natl Acad Sci USA. 2008;105(31):10925-10930. PubMed 18667694 ↗
[2]Heij L et al. Cibinetide (ARA-290) Improves Corneal Nerve Fiber Density and Symptoms in Sarcoidosis-Related Small Fiber Neuropathy: A Randomized Controlled Trial. Invest Ophthalmol Vis Sci. 2020. PubMed 32716524 ↗
Available via LHP — 10mg ($85)
KPV
Lys-Pro-Val · Alpha-MSH(11-13) · C-terminal MSH tripeptide
C-terminal tripeptide of α-MSH. Potent anti-inflammatory and antimicrobial activity without melanocortin receptor-mediated side effects of full-length α-MSH. Strong signal for IBD and gut inflammation.
Mechanism of Action
KPV is the C-terminal tripeptide of α-MSH, retaining its anti-inflammatory activity without the melanocortin receptor-mediated systemic effects of the full-length peptide. Mechanisms: direct intracellular signaling in epithelial and immune cells via a non-classical pathway; NF-κB inhibition reducing production of TNF-α, IL-1β, IL-6, and IL-8; antimicrobial peptide activity against gram-positive and gram-negative bacteria; and intestinal epithelial barrier strengthening. Particularly effective at reducing colonic inflammation in murine IBD models. The tripeptide is small enough to penetrate oral mucoadhesive formulations for GI-targeted delivery.
Primary Clinical Applications
Administration Routes
Oral (GI applications)Subcutaneous injectionTopical
Evidence Level
Strong preclinical; limited human data. Multiple murine colitis models show significant reduction in inflammatory markers and tissue damage. In vitro human cell studies confirm NF-κB inhibition and barrier-strengthening effects. Oral delivery systems (hydrogels, nanoparticles) under active investigation. Human clinical trials not yet completed.
Key Reference
[1]Cavagnini KS et al. Alpha-melanocyte-stimulating hormone peptides inhibit the production of pro-inflammatory cytokines and nitric oxide by activated microglia. J Neuroinflammation. 2010. PubMed 20105326 ↗
Available via LHP — 5mg ($60) · 10mg ($95) · "Klow" blend (BPC+GHK-Cu+TB500+KPV) $265
LL-37
Cathelicidin · CAP18/LL-37 · hCAP18 C-terminal peptide
Only human cathelicidin antimicrobial peptide. Broad-spectrum antimicrobial, anti-biofilm, and immunomodulatory activities. Deficient in certain skin conditions (eczema, rosacea, acne). Emerging wound care and cancer immunotherapy applications.
Mechanism of Action
LL-37 is a 37-amino acid cationic peptide — the only member of the cathelicidin family in humans. It is generated from the precursor protein hCAP18 by protease cleavage in neutrophil granules, keratinocytes, and epithelial cells. Actions: direct membrane disruption of bacterial, fungal, and viral cell walls via electrostatic interaction (effective against MRSA, P. aeruginosa, SARS-CoV-2); anti-biofilm activity; LPS neutralization reducing endotoxin-mediated inflammation; wound healing acceleration via keratinocyte migration, angiogenesis (VEGF), and re-epithelialization; immune modulation — chemotaxis of monocytes, T-cells; and emerging anti-tumor immune activation via toll-like receptor engagement.
Primary Clinical Applications
Administration Routes
TopicalSubcutaneous injectionInhalation (pulmonary)
Evidence Level
Strong mechanistic + preclinical; limited clinical RCTs. Well-characterized mechanism of action with extensive in vitro and in vivo data. Early-phase human wound healing trials show positive signals. LL-37 deficiency linked to eczema and increased skin infection susceptibility in observational studies. Pharmaceutical interest is high — delivery challenges (rapid in vivo degradation) have slowed clinical development.
Key Reference
[1]Vandamme D et al. A comprehensive summary of LL-37, the factotum human cathelicidin peptide. Cell Immunol. 2012;280(1):22-35. PubMed 23246639 ↗
Available via LHP — 5mg ($90)
Nootropics & Neuroregulatory Peptides
Russian-developed neuropeptides with anxiolytic and cognitive enhancement properties
Selank
TP-7 · Tuftsin analog · Heptapeptide-7
Synthetic analog of tuftsin (Thr-Lys-Pro-Arg-Pro-Gly-Pro). Developed by the Russian Institute of Molecular Genetics. Approved in Russia for anxiety and cognitive impairment. Anxiolytic without sedation or dependency.
Mechanism of Action
Selank is a heptapeptide derived from the immunomodulatory tuftsin tetrapeptide, extended to enhance metabolic stability. Primary mechanisms: GABA-A receptor modulation producing anxiolytic effects without benzodiazepine-like sedation or dependency; serotonin system stabilization; BDNF (brain-derived neurotrophic factor) upregulation supporting memory consolidation and synaptic plasticity; enkephalin enzyme inhibition prolonging endogenous opioid peptide activity; and immune modulation via tuftsin-like IL-6 pathway effects. Does not cause tolerance or physical dependency in animal models.
Primary Clinical Applications
Administration Routes
Intranasal (approved form)Subcutaneous injection
Evidence Level
Human clinical data from Russian trials. Approved in Russia (Selank, Phenylpiracetam formulations) for anxiety and neurological disorders. Phase II/III Russian RCTs confirm anxiolytic effects comparable to benzodiazepines without sedation or addiction. Western independent RCTs are limited. Most published data from Russian institutions.
Key References
[1]Semenova TP et al. Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress. Ross Fiziol Zh Im I M Sechenova. 2010. PubMed 21186737 ↗
[2]Zozulia AA et al. Efficacy and possible mechanisms of the anxiolytic action of a new peptide drug selank. Bull Exp Biol Med. 2001;131(3):241-245. PubMed 11402109 ↗
Regulatory status: Approved in Russia for anxiety and adaptive disorders. Not FDA-approved. Available via 503A compounding with physician Rx in the US.
Available via LHP — 5mg ($47.50) · 10mg ($70)
DSIP
Delta Sleep-Inducing Peptide · Nonapeptide-6
Endogenous neuropeptide originally isolated from rabbit cerebral venous blood during slow-wave sleep. Modulates sleep architecture, stress hormones, and HPA axis activity.
Mechanism of Action
DSIP is a naturally occurring nonapeptide first isolated by Monnier et al. (1977) from rabbit dialysate during slow-wave sleep. It acts on multiple systems: promotion of delta (slow-wave) sleep via direct CNS modulation; HPA axis suppression — reduces CRH, ACTH, and cortisol secretion; modulation of LH and GH pulsatility; and antioxidant and cytoprotective effects. It normalizes disrupted sleep architecture without causing pharmacological sedation. Also demonstrates anti-stress and adaptogenic properties by damping hyperactive HPA responses.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIV (research)
Evidence Level
Early human studies; not replicated in large RCTs. Original Swiss human trials (Schoenenberger et al., 1977-1983) demonstrated sleep-promoting effects with IV DSIP. Subsequent small human studies showed cortisol normalization and sleep improvement. Synthesis of evidence is complicated by DSIP's rapid degradation in plasma. Western large-scale RCTs have not been conducted.
Key Reference
[1]Schoenenberger GA et al. Characterization and properties of a delta-EEG-inducing peptide (DSIP). Pflugers Arch. 1977;369(2):99-109. PubMed 881843 ↗
Available via LHP — 5mg ($60) · 15mg ($150)
Semax
MEHFPGP · Heptapeptide ACTH(4-10) analog · N-Pro-Gly-Pro extended
Synthetic heptapeptide analog of ACTH(4-7) developed by the Russian Institute of Molecular Genetics. Approved in Russia for stroke, TBI, and cognitive impairment. BDNF and VEGF upregulation drives neuroprotective effects.
Mechanism of Action
Semax is a heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) based on the ACTH(4-10) fragment but modified to resist enzymatic degradation. Mechanisms: BDNF and NGF upregulation in the hippocampus and cortex, promoting neuronal survival and synaptic plasticity; VEGF induction supporting cerebral angiogenesis; melanocortin receptor modulation (MC4R) influencing attention and memory circuits; serotonin and dopamine system stabilization; and anti-inflammatory effects via reduction of pro-inflammatory cytokines after ischemic injury. Does not bind glucocorticoid receptors — no cortisol-like effects.
Primary Clinical Applications
Administration Routes
Intranasal (approved form)Subcutaneous injection
Evidence Level
Russian-approved; limited Western RCT data. Approved in Russia for ischemic stroke, cognitive impairment, and optic nerve disease. Multiple Russian clinical trials published in Russian journals. Western-indexed trials are limited. Mechanistic data (BDNF/VEGF induction) is robust and independently confirmed. Considered among the better-validated Russian neuropeptides.
Key References
[1]Inozemtsev AN et al. Semax peptide effects on experimental anxiety in mice. Bull Exp Biol Med. 2003;136(1):51-53. PubMed 14526084 ↗
[2]Dolotov OV et al. Semax, an Analog of ACTH(4–10), Regulates Expression of BDNF and Its Receptor TrkB in Rats. J Mol Neurosci. 2006;28:181-192. PubMed 16679563 ↗
Available via LHP — 5mg ($60) · 10mg ($100)
Dermatology & Cosmetic Peptides
Topical and injectable peptides for skin regeneration and anti-aging dermatology
Snap-8
Leuphasyl · Argireline extended · Octapeptide-3
8-amino acid analog of the N-terminal SNAP-25 protein. Competes with SNAP-25 for SNARE complex binding, reducing vesicle fusion and neurotransmitter release at the neuromuscular junction — topical alternative to botulinum toxin.
Mechanism of Action
Snap-8 is a synthetic octapeptide that mimics the N-terminal end of SNAP-25, a substrate for SNARE complex assembly. By competing for SNARE binding, it inhibits presynaptic vesicle fusion at cholinergic motor neuron terminals, reducing acetylcholine release and thereby relaxing superficial facial muscles involved in expression-line formation. Effect is localized to site of application; reversible; no systemic neurotoxicity. Clinical studies show approximately 63% reduction in wrinkle depth at optimal concentration (10 ppm) after 28 days of topical use.
Primary Clinical Applications
Administration Routes
Topical (cream/serum)
Evidence Level
Industry-sponsored clinical studies. 44-volunteer 28-day RCT reported 63% average reduction in wrinkle depth vs. placebo. Primary evidence is from cosmetic industry studies (not peer-reviewed RCTs in major journals). In vitro SNARE inhibition data is robust and mechanistically sound.
Available via LHP — 10mg ($60)
Hormonal & Reproductive Peptides
Melanocortin agonists and neuroendocrine peptides for sexual health and reproductive function
PT-141 (Bremelanotide)
Vyleesi (FDA-approved) · MC4R agonist · Melanocortin receptor agonist
FDA-approved melanocortin receptor agonist for hypoactive sexual desire disorder (HSDD) in premenopausal women. Also used off-label in men. Central (non-vascular) mechanism distinct from PDE5 inhibitors.
Mechanism of Action
PT-141 (bremelanotide) is a cyclic hepta-peptide melanocortin analog derived from Melanotan-II. Unlike PDE5 inhibitors which act on peripheral vasculature, PT-141 acts centrally via MC3R and MC4R receptors in the hypothalamus and limbic system, activating sexual arousal pathways independently of genital blood flow. This makes it effective for both men and women, including those who do not respond to sildenafil. Onset: 45–60 minutes. Duration: 12 hours. Approved dose: 1.75mg SQ.
Primary Clinical Applications
Administration Routes
Subcutaneous injection (approved)Intranasal (off-label)
Evidence Level
FDA-approved (Phase III data). RECONNECT trials: significant improvement in satisfying sexual events and Female Sexual Function Index vs. placebo. Common AEs: nausea, flushing, transient blood pressure elevation. FDA-approved August 2019 under brand name Vyleesi (Palatin Technologies / AMAG Pharmaceuticals).
Key References
[1]Clayton AH et al. Bremelanotide for Female Sexual Dysfunctions in Premenopausal Women (RECONNECT). Obstet Gynecol. 2016;128(3):536-547. PubMed 27500330 ↗
Regulatory status: FDA-approved as Vyleesi for HSDD in premenopausal women (2019). Compounded bremelanotide available via 503A for broader clinical use including off-label male sexual dysfunction.
Available via LHP — 10mg ($100)
KissPeptin-10
Metastin(45-54) · KP-10 · KISS1 gene product
C-terminal decapeptide of kisspeptin-54, the endogenous regulator of the HPG axis. Directly stimulates GnRH pulse release, LH, FSH, and downstream sex steroid production. Key diagnostic and therapeutic tool in reproductive medicine.
Mechanism of Action
Kisspeptin-10 is the minimum active fragment of kisspeptin, binding GPR54 (Kiss1R) receptors on GnRH neurons in the hypothalamic arcuate nucleus and anteroventral periventricular nucleus. GPR54 activation triggers pulsatile GnRH release, the master switch of the HPG axis, producing downstream LH and FSH surges. In men: increases testosterone via LH stimulation. In women: triggers ovulatory LH surge. KP-10 is the most potent and shortest kisspeptin fragment with full biological activity. It has established diagnostic utility for differentiating hypothalamic from pituitary causes of hypogonadism, and therapeutic potential for HH and fertility.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIV infusion (diagnostic)
Evidence Level
Multiple human RCTs; extensive reproductive endocrinology data. Dhillo et al. Cambridge/Imperial College series: multiple RCTs confirming LH, FSH, and testosterone elevation in hypogonadal men and ovulation induction in women. Phase II IVF trigger data. Kisspeptin analogs in Phase III development. Strongest evidence base for reproductive applications in the LHP hormonal catalog.
Key References
[1]Dhillo WS et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. J Clin Endocrinol Metab. 2005;90(12):6609-6615. PubMed 16204359 ↗
[2]Jayasena CN et al. Subcutaneous infusion of kisspeptin-54 stimulates gonadotrophin release in women and the response is modulated by sex steroid feedback. J Clin Endocrinol Metab. 2011;96(9):E1492-E1501. PubMed 21816790 ↗
Available via LHP — 5mg ($70) · 10mg ($100)
Oxytocin
Pitocin (synthetic) · Bonding hormone · Nonapeptide neurohormone
Endogenous 9-amino acid hypothalamic neuropeptide and neurohormone. FDA-approved for obstetric indications. Expanding evidence for social bonding, anxiety, autism spectrum, and metabolic applications via nasal or injectable routes.
Mechanism of Action
Oxytocin is a cyclic nonapeptide (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2) produced in the paraventricular and supraoptic nuclei of the hypothalamus. Peripheral actions: uterine contraction (FDA-approved obstetric use); milk ejection. Central/neuromodulatory actions: binding to OT receptors in limbic system, amygdala, and brainstem producing anxiolysis, social bonding facilitation, and trust enhancement; amygdala fear response attenuation; HPA axis modulation (cortisol reduction); and emerging metabolic effects including appetite suppression, fat utilization, and leptin sensitization via hypothalamic circuits.
Primary Clinical Applications
Administration Routes
Intranasal (central effect)Subcutaneous injectionIV (obstetric — approved)
Evidence Level
FDA-approved (obstetric); mixed evidence for off-label CNS applications. Intranasal oxytocin RCTs in social anxiety, ASD, and PTSD have shown variable results — positive signals in meta-analyses but inconsistent across individual trials (likely due to dose variability and central penetration differences). Metabolic effects (appetite, fat) confirmed in murine models; early human metabolic data exists. Active area of pharmaceutical development.
Key References
[1]Kosfeld M et al. Oxytocin increases trust in humans. Nature. 2005;435(7042):673-676. PubMed 15931222 ↗
[2]Macdonald K, Macdonald TM. The peptide that binds: a systematic review of oxytocin and its prosocial effects in humans. Harv Rev Psychiatry. 2010;18(1):1-21. PubMed 20047458 ↗
Available via LHP — 10mg ($70) · 50mg ($199)
Fat-Loss & Metabolic Modulators
Growth hormone fragments, AMPK activators, and adipose-targeted peptides
AOD9604
Anti-Obesity Drug 9604 · hGH fragment 177-191
C-terminal fragment of human growth hormone (aa 177-191). Retains the lipolytic activity of hGH without its anabolic/diabetogenic effects. FDA GRAS status obtained 2014. Extensive safety profile.
Mechanism of Action
AOD9604 is the 16-amino acid C-terminal fragment of hGH (residues 177-191), containing the region responsible for hGH's fat-metabolizing activity. Mechanism: beta-3 adrenergic receptor stimulation in adipocytes, activating cyclic AMP and hormone-sensitive lipase to increase lipolysis; inhibition of lipogenesis (fat storage); does not stimulate IGF-1 production, does not affect blood glucose, and does not cause insulin resistance — critical advantages over full hGH. Recent research suggests additional cartilage regeneration effects via VEGF and TGF-β pathways, expanding potential applications beyond fat loss.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionOral (FDA GRAS approved form)
Evidence Level
Phase II trials completed; FDA GRAS designation. Merck developed AOD9604 through Phase II trials (METAOD studies) showing modest but significant fat loss. FDA GRAS (Generally Recognized as Safe) status obtained 2014 for oral dietary supplement use. Injectable compounded form widely used in clinical practice. Phase III trials for obesity did not proceed; cartilage repair Phase IIb (OA201) showed positive signal.
Key References
[1]Heffernan MA et al. The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knockout mice. Endocrinology. 2001;142(12):5182-5189. PubMed 11713213 ↗
Available via LHP — 5mg ($65) · 10mg ($100)
5-Amino-1MQ
5-amino-1-methylquinolinium · NNMT inhibitor
Small molecule inhibitor of Nicotinamide N-methyltransferase (NNMT) — an enzyme overexpressed in adipose tissue during obesity. Raises intracellular SAM and NAD+ levels, suppressing fat cell differentiation and promoting metabolic health.
Mechanism of Action
NNMT methylates nicotinamide using S-adenosylmethionine (SAM), producing 1-methylnicotinamide and S-adenosylhomocysteine. In obese adipose tissue, elevated NNMT activity depletes SAM and indirectly depletes NAD+ precursors — creating a metabolically unfavorable state that promotes further fat cell expansion. 5-Amino-1MQ selectively inhibits NNMT, restoring SAM levels, raising the SAM/SAH ratio, elevating intracellular NAD+ pools, and inhibiting adipocyte differentiation. In diet-induced obese mice: significant reduction in adipose tissue mass, improved insulin sensitivity, and reduced lipid droplet accumulation — without changes in food intake.
Primary Research Applications
Administration Routes
Subcutaneous injectionOral (investigational)
Evidence Level
Preclinical only — no published human trials. Gao et al. (Nat Commun. 2019) demonstrated NNMT inhibitor effects in diet-induced obese mice with compelling metabolic data. No human dose-finding or safety trials published. Growing clinical interest as an adjunct to GLP-1 programs. Experimental.
Key Reference
[1]Gao Z et al. NNMT Contributes to High Fat Diet-Induced Depletion of Hepatic NAD+. Front Endocrinol. 2019. PubMed 31998229 ↗
Available via LHP — 5mg ($85)
AICAR
5-Aminoimidazole-4-carboxamide ribonucleotide · AICA ribonucleotide · Acadesine
AMP analog and potent AMPK activator. Acts as an endurance-mimicking "exercise in a molecule" — improves fat oxidation, insulin sensitivity, and mitochondrial biogenesis without exercise. Phase III data in CLL.
Mechanism of Action
AICAR is a nucleoside that is phosphorylated intracellularly to ZMP, an AMP analog that directly activates AMP-activated protein kinase (AMPK) — the cell's master energy sensor. AMPK activation produces a cascade mimicking the cellular state of exercise: increased GLUT4 translocation and glucose uptake; enhanced fatty acid oxidation in muscle and liver; PGC-1α upregulation driving mitochondrial biogenesis; mTOR inhibition reducing anabolic/inflammatory signaling; and FOXO3 activation supporting autophagy. Also inhibits de novo lipogenesis. At the macro level, produces endurance and metabolic improvements similar to aerobic training.
Primary Clinical Applications
Administration Routes
IV infusion (clinical trials)Subcutaneous injectionOral (lower bioavailability)
Evidence Level
Phase II/III data in multiple indications. WING trial (coronary artery bypass): Phase III in cardiac protection. Phase III in relapsed/refractory CLL (acadesine). Extensive human metabolic data from exercise physiology research. WADA banned substance in competitive sports — confirms its exercise-mimicking efficacy. Metabolic applications are off-label but well-supported mechanistically.
Key Reference
[1]Narkar VA et al. AMPK and PPARδ agonists are exercise mimetics. Cell. 2008;134(3):405-415. PubMed 18674809 ↗
Note: AICAR is a WADA-prohibited substance in competitive sports. Confirm athlete status before prescribing.
Available via LHP — 50mg ($55)
Adipotide
FTPP · Fat-targeting pro-apoptotic peptide
Proapoptotic peptide that selectively targets and destroys the blood vessels supplying white adipose tissue. Produced dramatic fat loss in obese rhesus monkeys. Human data limited but highly promising mechanism.
Mechanism of Action
Adipotide (CKGGRAKDC-GG-KLAKLAKKLAKLAK) is a chimeric peptide composed of two functional domains: a targeting domain (CKGGRAKDC) that binds prohibitin on the surface of blood vessel endothelial cells specifically in white adipose tissue vasculature; and a pro-apoptotic domain (KLAKLAK)₂ that disrupts mitochondrial membranes to trigger cell death. By destroying the blood supply to adipose tissue, it causes adipocyte death from ischemia. In obese rhesus monkeys: ~11% body weight reduction in 28 days with improvement in insulin sensitivity, kidney function, and metabolic markers. Highly targeted — does not affect brown fat, muscle, or other tissue vasculature at tested doses.
Primary Research Applications
Administration Routes
Subcutaneous injection
Evidence Level
Primate data only — no published human trials. Daquinag et al. and Barnhart et al. studies in obese mice and rhesus monkeys showed dramatic fat reduction. Phase I trial in prostate cancer patients included adipotide as secondary endpoint — kidney toxicity signal observed at high doses that stalled obesity-indication development. Highly experimental. Dose and safety profile in humans not established for fat-loss applications.
Key Reference
[1]Barnhart KF et al. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med. 2011;3(108):108ra112. PubMed 22072638 ↗
Highly experimental: Kidney toxicity observed at high doses in primate studies. No established human dosing or safety profile for obesity applications. Extreme caution and close clinical monitoring required.
Available via LHP — 2mg ($65) · 5mg ($120)
Pigmentation Peptides
Melanocortin receptor agonists for photoprotection, tanning, and libido modulation
Melanotan-1
Afamelanotide · Scenesse · [Nle4,D-Phe7]-alpha-MSH
Synthetic alpha-MSH analog. FDA and EMA approved as Scenesse (implant) for erythropoietic protoporphyria (EPP) — the first approved melanocortin agonist. Induces eumelanin pigmentation without UV exposure for photoprotection.
Mechanism of Action
Melanotan-1 (afamelanotide) is a linear alpha-MSH analog with Nle4 and D-Phe7 substitutions that enhance metabolic stability and receptor binding affinity. It activates MC1R on melanocytes, stimulating cAMP-dependent tyrosinase activation and subsequent production of eumelanin (brown/black melanin) — the photoprotective form. This produces photoprotective tanning independent of UV exposure. MC1R is also expressed in immune cells, providing anti-inflammatory effects. Minimal MC3R/MC4R activity compared to Melanotan-2 — essentially no libido or erection effects, making it a cleaner photoprotection agent.
Primary Clinical Applications
Administration Routes
Subcutaneous implant (approved)Subcutaneous injection (off-label)
Evidence Level
FDA and EMA approved (Scenesse/afamelanotide) for EPP. Phase III RCTs confirmed increased pain-free sun exposure in EPP patients. Extensive Phase II data for vitiligo and solar urticaria. Robust safety profile established. Compounded injectable form used off-label for cosmetic purposes — same molecule, different delivery.
Key Reference
[1]Langendonk JG et al. Afamelanotide for Erythropoietic Protoporphyria. N Engl J Med. 2015;373(1):48-59. PubMed 26132941 ↗
Available via LHP — 10mg ($130)
Melanotan-2
MT-II · [Nle4,D-Phe7]-alpha-MSH cyclic analog · Bremelanotide precursor
Cyclic synthetic alpha-MSH analog with broad melanocortin receptor activity (MC1R, MC3R, MC4R). Produces tanning, appetite suppression, and sexual arousal effects simultaneously. PT-141 (Vyleesi) was derived from MT-II by removing the tanning activity.
Mechanism of Action
MT-II is a cyclic heptapeptide with broad melanocortin receptor agonism: MC1R (melanocyte stimulation → eumelanin pigmentation and tanning); MC3R (energy balance, appetite suppression, cardiovascular); MC4R (hypothalamic sexual arousal, erectile function, appetite). This combined receptor profile produces three simultaneous effects: tanning/photoprotection, libido/erection stimulation (same mechanism as PT-141/Vyleesi), and appetite reduction. PT-141 was engineered from MT-II by removing the cyclic structure that confers MC1R tanning activity, isolating the sexual function component. Side effects include nausea, facial flushing, and spontaneous erections at higher doses.
Primary Clinical Applications
Administration Routes
Subcutaneous injectionIntranasal
Evidence Level
Phase II trials; not FDA-approved. Phase II data confirms tanning, erectile, and appetite effects. Not advanced to FDA approval for any indication — PT-141 was the approved derivative (for HSDD). Dermatological concern: may stimulate atypical nevus growth at high doses. Extensive preclinical and Phase II human data exist.
Note: MT-II has broader receptor activity than PT-141 including tanning effects. Patients with personal or family history of melanoma should be approached with caution given MC1R stimulation and theoretical risk of stimulating atypical nevi.
Available via LHP — 10mg ($130)
Next-Generation Metabolic Peptides
Amylin analogs and GLP-1/glucagon dual agonists in active Phase II–III development
Cagrilintide
AM833 · Long-acting amylin analog · Amylin/CGRP receptor agonist
Once-weekly long-acting amylin analog developed by Novo Nordisk. In the CagriSema combination with semaglutide, Phase III data shows up to 22.7% weight loss — the strongest combination metabolic signal in clinical trials to date.
Mechanism of Action
Amylin is a pancreatic peptide co-secreted with insulin by beta-cells that acts on amylin receptors (AMY1-3) in the hypothalamus and area postrema to produce satiety, slow gastric emptying, and suppress glucagon. Cagrilintide is an amylin analog modified for once-weekly dosing (extended half-life via fatty-acid conjugation). Its mechanism is synergistic but complementary to GLP-1 receptor agonism — amylin acts on different hypothalamic circuits, particularly brainstem satiety pathways, providing additive appetite suppression without receptor overlap. The CagriSema combination (cagrilintide + semaglutide 2.4mg) produced 22.7% weight loss at 68 weeks in Phase IIb — substantially exceeding semaglutide alone (~15%).
Primary Clinical Applications
Administration Routes
Subcutaneous injection (weekly)
Evidence Level
Phase II completed; Phase III ongoing (REDEFINE program). REDEFINE 1 (Phase III, obesity): 22.7% mean weight loss at 68 weeks with CagriSema vs 8.1% placebo. REDEFINE 2 (T2DM) ongoing. No FDA approval yet — Phase III readout expected 2025-2026. Compounded cagrilintide or CagriSema combination available via LHP 503A now — branded product does not yet exist.
Key Reference
[1]Frias JP et al. Efficacy and Safety of Co-administered Once-weekly Cagrilintide 2.4 mg With Once-weekly Semaglutide 2.4 mg in Type 2 Diabetes. Lancet. 2023;402:720-730. PubMed 37352886 ↗
Available via LHP — 5mg ($125) · 10mg ($175) · Cagrilintide + Semaglutide 5mg+5mg combo ($150)
Survodutide
BI 456906 · GLP-1R / GCGR dual agonist
Once-weekly GLP-1R and glucagon receptor (GCGR) dual agonist. Glucagon co-activation drives thermogenesis and hepatic fat reduction — strong signal for MASH/NAFLD beyond obesity. Phase III in MASH and obesity.
Mechanism of Action
Survodutide is a once-weekly injectable dual agonist with balanced activity at GLP-1R and GCGR. GLP-1R agonism provides appetite suppression, insulin sensitization, and cardiovascular benefit. GCGR co-activation adds: increased thermogenesis via brown adipose tissue activation; hepatic fat oxidation and reduced de novo lipogenesis — particularly relevant for MASH; energy expenditure enhancement beyond appetite suppression alone. The dual hepatic mechanism (GLP-1R + GCGR) makes survodutide particularly promising for MASH/NAFLD where hepatic steatosis is the primary target. Phase II MASH data showed significant liver fat reduction and fibrosis improvement.
Primary Clinical Applications
Administration Routes
Subcutaneous injection (weekly)
Evidence Level
Phase II completed; Phase III underway. Phase II MASH trial: significant reduction in liver fat, improvement in liver histology, and weight loss vs. placebo. Phase II obesity: ~14.9% weight loss at 46 weeks. Phase III trials (SYNCHRONIZE program) ongoing for MASH and obesity. No FDA approval yet — next-generation metabolic agent available now via LHP compounding ahead of branded product.
Key Reference
[1]Loomba R et al. Randomised, placebo-controlled phase 2 trial of survodutide for metabolic dysfunction-associated steatohepatitis. J Hepatol. 2024;81(2):208-219. PubMed 38499179 ↗
Available via LHP — 10mg ($150)
LHP Regenerative Blends
Pre-formulated combinations optimized for synergistic tissue repair, wound healing, and recovery protocols
"Wolverine" — BPC-157 + TB-500
The Regeneration Stack · Tissue Repair Combination Protocol
The most widely used peptide repair combination in clinical practice. BPC-157 drives angiogenesis and fibroblast activation at the injury site; TB-500 (Tβ4) drives systemic actin remodeling, cell migration, and anti-inflammatory resolution. Complementary and potentially synergistic mechanisms.
Rationale for Combination
BPC-157 and TB-500 address tissue repair through fundamentally different but complementary pathways. BPC-157 works primarily at the local injury level via VEGFR2 and eNOS activation — driving blood vessel formation and fibroblast migration into the wound. TB-500 works systemically and locally via actin dynamics — enabling cell migration across tissue planes, reducing inflammation via NF-κB inhibition, and activating stem cell homing. Together, they address both the structural (BPC-157: vasculature, matrix) and cellular mobilization (TB-500: actin, stem cells) components of healing, providing theoretical synergy that is supported by the dramatic efficacy observed anecdotally in clinical practice, though no head-to-head combination RCTs exist.
Primary Clinical Applications
Dosing Options Available
Three sizes available to match protocol duration and patient needs. Typical acute injury protocols: 5mg+5mg or 7mg+7mg for 4–8 week cycles. Severe injuries or post-surgical: 10mg+10mg for full course.
Administration
Subcutaneous injectionNear injury site preferredTypically 2-3x/week
Evidence note: Both compounds have independent preclinical evidence; combination is extrapolated from mechanism. No combination RCT exists. Clinical use reflects established practitioner protocols developed over years of practical application.
Available via LHP — 5mg+5mg ($100) · 7mg+7mg ($120) · 10mg+10mg ($135)
"Glow" — BPC-157 + GHK-Cu + TB-500
Triple regenerative blend · Aesthetic + Healing combination
Adds GHK-Cu's collagen remodeling and dermal regeneration profile to the Wolverine stack. Targeted at patients combining systemic tissue repair goals with skin rejuvenation — post-procedure recovery, aesthetic medicine patients, and anti-aging protocols.
Rationale for Three-Component Combination
The Glow blend adds GHK-Cu to the BPC-157/TB-500 base. GHK-Cu contributes: collagen and elastin synthesis in dermal fibroblasts, MMP/TIMP regulation for matrix remodeling, and antioxidant gene upregulation (Broad Institute CMap data: 31.2% of human genes modulated ≥50%). For aesthetic medicine patients — particularly those recovering from laser resurfacing, microneedling, or dermal procedures — the dermal regeneration effects of GHK-Cu complement the vascular and structural repair driven by BPC-157 and TB-500. The combination addresses healing at three levels: vasculature (BPC-157), cellular mobilization (TB-500), and dermal matrix remodeling (GHK-Cu).
Primary Clinical Applications
Composition
BPC-157 10mg + GHK-Cu 50mg + TB-500 10mg = 70mg total in lyophilized form. Reconstituted together for combined administration.
Administration
Subcutaneous injectionNear target tissue
Available via LHP — 70mg total ($230) · "Klow" variant adds KPV ($265)
"Klow" — BPC-157 + GHK-Cu + TB-500 + KPV
Quad regenerative blend · Anti-inflammatory healing combination
The Glow blend extended with KPV for patients with significant inflammatory component — IBD, autoimmune skin conditions, post-surgical inflammation, or GI-involved healing. KPV's NF-κB inhibition addresses the inflammatory environment that often impairs the healing cascade.
Rationale for KPV Addition
KPV (Lys-Pro-Val), the C-terminal tripeptide of α-MSH, is the most potent anti-inflammatory component of the melanocortin system without the receptor-wide side effects of full-length α-MSH. Its addition to the Glow stack specifically addresses the inflammatory microenvironment that can impair all three regenerative mechanisms: excessive NF-κB activity and SASP-like cytokine release (TNF-α, IL-1β, IL-6) directly inhibit fibroblast function, impair angiogenesis, and prevent proper matrix deposition. By suppressing this inflammatory background with KPV, the BPC-157/TB-500/GHK-Cu regenerative machinery can operate in a more permissive environment. Particularly relevant for: IBD patients, autoimmune skin disease, diabetic wound healing, and any patient with chronic low-grade systemic inflammation.
Primary Clinical Applications
Composition
BPC-157 10mg + GHK-Cu 50mg + TB-500 10mg + KPV 10mg = 80mg total in lyophilized form.
Administration
Subcutaneous injectionOral (for GI applications — KPV is orally active)
Available via LHP — 80mg total ($265)