Peptide Profile
Alpha-MSH
Alpha-Melanocyte Stimulating Hormone · α-MSH
α-Melanocyte-stimulating hormone (α-MSH) is an endogenous 13-amino-acid peptide derived from proteolytic processing of proopiomelanocortin (POMC) that acts through melanocortin receptors (MC1R–MC5R), with biological roles…
- Half-life
- ~3-5 minutes (plasma)
- Routes
- subcutaneous, intranasal
Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.
Educational research tools — not medical advice.
What Alpha-MSH is
About Alpha-MSH
Melanocortin peptide; activates MC1R (pigmentation/anti-inflammatory), MC3R (energy balance), MC4R (appetite); suppresses NF-κB and pro-inflammatory cytokines
α-Melanocyte-stimulating hormone (α-MSH) is an endogenous 13-amino-acid peptide derived from proteolytic processing of proopiomelanocortin (POMC) that acts through melanocortin receptors (MC1R–MC5R), with biological roles including skin pigmentation, anti-inflammatory signaling, thermoregulation, and energy homeostasis. Its anti-inflammatory actions are mediated principally through MC1R and MC3R activation, leading to inhibition of NF-κB-dependent cytokine production, reduction of pro-inflammatory mediators including IL-1β and TNF-α, and modulation of leukocyte activity in both peripheral and central nervous system compartments. Research published in the Annals of the New York Academy of Sciences has characterized the mechanisms of α-MSH's anti-inflammatory activity in vivo and in vitro, and subsequent work has described new insights into its immunomodulatory functions and therapeutic potential in inflammatory conditions. α-MSH is a research compound with no FDA approval for any indication; no human clinical trials have established safety or efficacy for exogenous α-MSH administration in anti-inflammatory, neuroprotective, or other therapeutic contexts. Alpha-MSH and the melanocortin peptide family α-MSH is the prototype endogenous ligand for the melanocortin receptor family — five receptors (MC1R–MC5R) with distinct tissue distribution and functions. The pharmacological development of synthetic melanocortin analogues has produced several clinically and commercially relevant compounds derived from or inspired by α-MSH: Melanotan I (afamelanotide, MC1R-selective, approved as Scenesse for erythropoietic protoporphyria), Melanotan II (non-selective, superpotent, never approved; extensively used in research), and PT-141/bremelanotide (cyclized Melanotan II analogue, FDA-approved as Vyleesi for female hypoactive sexual desire disorder via MC3R/MC4R). α-MSH itself serves as the structural reference point for this lineage — the pharmacophore binding sequence (His-Phe-Arg-Trp) shared by all active melanocortin analogues is derived from α-MSH residues 6–9. Appetite regulation and obesity research: α-MSH's role in energy homeostasis is mediated through MC4R activation in the hypothalamus, where it acts as an endogenous satiety signal opposing the appetitive effects of AgRP (agouti-related protein). Loss-of-function MC4R mutations are the most common monogenic cause of severe early-onset obesity, establishing the α-MSH/MC4R pathway as a validated target for pharmacological weight management. Setmelanotide (Imcivree), an MC4R agonist, is FDA-approved for obesity caused by MC4R pathway deficiency mutations (POMC deficiency, PCSK1 deficiency, leptin receptor deficiency) — a direct pharmacological descendant of the α-MSH mechanism.
Alpha-MSH Benefits & Research Areas
Research Signals
Population research notes
These signals reflect research interest areas, not treatment indications.
Alpha-MSH half-life calculator
Compound & timing
Plasma clearance only: this reflects how long the compound is detectable in blood plasma — biological effects can outlast plasma levels.
Model: single-dose, first-order (single-compartment) estimate. Real clearance is multi-compartment and varies by individual and route.
What the evidence says about Alpha-MSH
Research Evidence
based on 12 studies · most recent 2026
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Not Evaluated
Endogenous 13-aa neuropeptide. No FDA-approved drug. Bremelanotide (PT-141/Vyleesi) is an approved derivative but a distinct compound. Not on FDA 503A bulks list. Research use only.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
12 sources cited · 12 weak
3 Reviews · 8 Animals · 1 In vitro
Preclinical assessment of (177)Lu-DOTA-Pip-Nle-CycMSH(hex): In vivo evaluation and human dosimetry estimation.
Appl Radiat Isot · 2026
Research found that 177Lu-DOTA-Pip-Nle-CycMSH(hex), a radiolabeled alpha-MSH analogue, demonstrated high affinity for melanocortin-1 receptors, selective tumor targeting in melanoma models, and favorable dosimetry profiles comparable to FDA-approved radiopharmaceuticals. This study demonstrated the compound's potential as a candidate for further development in melanoma-targeted radionuclide therapy based on its stability, receptor binding, cellular uptake, and safety dosimetry estimates.
Antrodia cinnamomea extract exhibits anti-melanogenic and anti-photoaging effects: potential for cosmetic and dermatological applications.
Sci Rep · 2026
Research found that Antrodia cinnamomea extract suppresses melanin production and tyrosinase activity in alpha-MSH-stimulated melanocytes by downregulating key pigmentation genes and inhibiting the PKA/cAMP/CREB signaling pathway. This study demonstrated that the extract also protects skin fibroblasts against UV-induced photoaging by reducing reactive oxygen species and decreasing the expression of matrix metalloproteinases and inflammatory cytokines, while maintaining safety and efficacy when formulated for cosmetic use.
Depigmenting Effects of Vitex rotundifolia Cone Essential Oil in Melanocytes and Its Chemical Composition.
Chem Biodivers · 2026
Research found that Vitex rotundifolia cone essential oil suppressed melanin synthesis and transport in melanocytes by inhibiting tyrosinase enzyme activity and reducing expression of melanin-related proteins (MITF, tyrosinase, and TRP-2) in alpha-MSH-stimulated cells. This study demonstrated that the essential oil's anti-pigmentation effects involved activation of specific cellular signaling pathways (p38 MAPK and ERK1/2) and decreased expression of proteins involved in melanin transfer between cells.
Show 9 more sources ↓
Hypothalamic orexigenic and anorexigenic neuropeptides in the rotenone model of Parkinson's disease.
Sci Rep · 2026
This study demonstrated that rotenone-induced Parkinson's disease in rats caused reduced expression of multiple appetite-regulating neuropeptides, including Alpha-MSH (derived from proopiomelanocortin), without causing actual neuron loss in the hypothalamus. Researchers observed that standard anti-Parkinson's therapy combined with antidepressant medication failed to restore these neuropeptide expression changes, suggesting that appetite dysregulation in Parkinson's disease involves complex functional alterations that are not addressed by conventional treatments.
Baeckea frutescens Suppresses Melanogenesis via Modulation of PKA/CREB and ERK/MAPK Pathways: Insights from Cellular, Zebrafish, and In Silico Analyses.
Molecules · 2026
Research found that Baeckea frutescens extract suppressed melanin production in cells stimulated with alpha-melanocyte-stimulating hormone (α-MSH) by reducing tyrosinase activity and downregulating key melanogenic proteins through modulation of the PKA/CREB and ERK/MAPK signaling pathways. This study demonstrated that the plant extract also reduced melanin accumulation in zebrafish embryos, suggesting potential anti-melanogenic mechanisms involving multiple molecular targets.
Cyperenoic acid from Gentiana kurroo suppresses Melanogenesis via modulation of MITF without altering ERK and CREB phosphorylation, with predicted interaction at the MITF kink pocket.
Fitoterapia · 2026
Skin-Protective Activities of Dioscorea batatas Decne Peel Extracts with Differential Phenanthrene Contents.
Antioxidants (Basel) · 2026
Tetrahedral framework nucleic acids carrying tranexamic acid to alleviate ultraviolet B-induced skin pigmentation.
Mater Today Bio · 2026
This study demonstrated that tetrahedral framework nucleic acids (tFNAs) enhanced the delivery and anti-pigmentation activity of tranexamic acid, reducing melanin production in cells stimulated by alpha-MSH and improving depigmentation in a UVB-induced mouse skin model. Researchers observed that this nanoparticle-based formulation suppressed key signaling pathways involved in melanin synthesis while showing improved tolerability compared to conventional approaches.
Bioactive Lipid Mediator Resolvin D5 Suppresses Melanogenesis in α-MSH-Stimulated B16F10 Cells via ROS-Associated p38/β-Catenin/MITF Regulation.
J Microbiol Biotechnol · 2026
Melanophore physiology and adrenergic receptor signaling in zebrafish (Danio rerio).
Fish Physiol Biochem · 2026
New insights into the functions of alpha-MSH and related peptides in the immune system
Annals of the New York Academy of Sciences · 2003
This review describes how alpha-MSH and its tripeptide fragment KPV suppress inflammatory cytokine production, downregulate costimulatory molecules on antigen-presenting cells via melanocortin-1 receptor binding, and induce antigen-specific tolerance in mouse models, positioning alpha-MSH as a candidate immunomodulatory agent for allergic and autoimmune conditions.
Mechanisms of antiinflammatory action of alpha-MSH peptides. In vivo and in vitro evidence
Annals of the New York Academy of Sciences · 1999
This review summarizes in vivo and in vitro evidence that alpha-MSH modulates inflammation via peripheral and central mechanisms including inhibition of NF-κB activation in immune cells, reduction of proinflammatory cytokine production, and activation of descending anti-inflammatory neural pathways, with actions conserved across diverse inflammatory models.
Alpha-MSH Side Effects & Safety Considerations
Research-use compound with limited human data. Evidence strength varies — see the Evidence section.
Reported (unverified — pending clinical review)
No established clinical contraindications
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
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Frequently Asked Questions — Alpha-MSH
α-Melanocyte-stimulating hormone (α-MSH) is an endogenous 13-amino-acid peptide derived from proteolytic processing of proopiomelanocortin (POMC) that acts through melanocortin receptors (MC1R–MC5R), with biological roles including skin pigmentation, anti-inflammatory signaling, thermoregulation, and energy homeostasis. Its anti-inflammatory actions are mediated principally through MC1R and MC3R activation, leading to inhibition of NF-κB-dependent cytokine production, reduction of pro-inflammatory mediators including IL-1β and TNF-α, and modulation of leukocyte activity in both peripheral and central nervous system compartments.
anti-inflammatory, appetite suppression, thermoregulation, skin pigmentation.
Research on Alpha-MSH primarily documents effects related to anti-inflammatory and appetite suppression and thermoregulation and skin pigmentation. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
Reported contraindications and considerations for Alpha-MSH include melanoma history, uncontrolled hypertension. This is educational information only — consult a qualified healthcare professional before use.
For Alpha-MSH, its FDA status is not evaluated by the FDA, and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
How to get Alpha-MSH
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