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The 2026 WADA Prohibited List explicitly includes activin receptor IIB competitors, such as decoy activin receptors, with ACE-031 given as a named example. Anti-doping prohibition is separate from FDA approval and clinical efficacy.

Testing of 14 black-market products sold as ACE-031 found major identity failures; 12 contained ACVR2B-immunoreactive material, but analyses indicated full-length activin receptor IIB rather than authentic ACE-031 Fc-fusion protein.

ACE-031 was studied in ambulatory boys with Duchenne muscular dystrophy. The program identified pharmacodynamic muscle effects but the trial was terminated after safety findings including epistaxis and telangiectasias.

ACE-031, an activin receptor type IIB-Fc fusion protein, produced dose-dependent increases in lean body mass and thigh muscle volume after a single dose in healthy postmenopausal women. The study was primarily a safety, pharmacokinetic, and pharmacodynamic study and did not establish a therapeutic or performance-enhancement indication.

A review of myostatin/ActRIIB-pathway inhibitors situates ACE-031 as a broad soluble ActRIIB ligand trap distinct from selective myostatin-only antibodies, and summarizes that its Duchenne muscular dystrophy development program was discontinued after safety findings. The review does not establish that ACE-031, ACE-083, or other ActRIIB/myostatin-pathway agents are interchangeable or that any is approved or safe for human muscle-building use.

Sponsor newsroom announcement describing dosing of the first patient in the Phase I Prohibitin-TP01/Adipotide study. Development-context material only -- not a peer-reviewed report of human weight-loss efficacy or outcome data, and registry status plus a company announcement do not by themselves establish published human efficacy.

NCI's Drug Dictionary describes prohibitin-targeting peptide 1 (Adipotide/Prohibitin-TP01) as an investigational chimeric peptidomimetic that combines a prohibitin-targeting domain with a proapoptotic sequence and notes potential antineoplastic activity. NCI does not describe an FDA-approved product or an established human obesity indication.

The initial 2019 SCENESSE prescribing information summarizes two vehicle-controlled EPP trials: Study CUV039 (93 subjects) reported median pain-free direct-sunlight time over 180 days of 64.1 hours with SCENESSE versus 40.5 hours with vehicle; Study CUV029 (74 subjects) reported 6.0 hours versus 0.75 hours under a narrower recording definition. The label lists common adverse reactions (implant-site reactions, nausea, oropharyngeal pain, cough, fatigue, dizziness, skin hyperpigmentation, somnolence, melanocytic nevus, respiratory-tract infection, skin irritation), recommends twice-yearly full-body skin examinations, and states that pregnancy data are inadequate, lactation data are absent, pediatric safety/efficacy are not established, renal/hepatic pharmacokinetic effects are unknown, no drug-interaction studies were conducted, and carcinogenicity studies were not conducted.

PubChem records identify AHK-Cu (the copper complex of L-alanyl-L-histidyl-L-lysine) and AHK-Cu hydrochloride as distinct chemical substance records. A database identity record is not FDA approval or clinical validation.

PubChem's GHK-Cu / prezatide copper record establishes GHK-Cu as a distinct chemical substance from AHK-Cu. Replacing the N-terminal glycine of GHK with alanine produces a different tripeptide; this record is cited for identity-boundary purposes only, not as AHK-Cu evidence.

FDA lists AOD-9604 among bulk substances for which compounded drug use may present significant safety risks and notes serious adverse events that may be associated with AOD-9604, while stating causality is not clear. This is a regulatory safety signal and not proof of a specific causal toxicity mechanism.

FDA's briefing document describes AOD-9604 free base as a 16-amino-acid peptide corresponding to hGH 177-191 with an additional N-terminal tyrosine and evaluates AOD-9604-related bulk substances for the 503A Bulks List. FDA proposed that AOD-9604 free base and acetate not be included on that list.

FDA's December 2024 review proposed that AOD-9604 free base and acetate not be added to the 503A Bulks List, citing inadequate physical and chemical characterization, inconsistent substance identity, lack of evidence of obesity effectiveness, limited safety information, absent human subcutaneous and transdermal data, potential immunogenicity and aggregation, peptide-related impurities, inadequate injectable endotoxin information, and nonclinical bone, liver, and equivocal genotoxicity signals.

The registered study plan identifies LAT8881 as Tyr-hGH177-191, formerly AOD9604, and reports six prior obesity trials involving 936 subjects, with more than 700 subjects receiving oral LAT8881. The final obesity efficacy study did not meet its primary endpoint, and development for the obesity indication ended in 2007.

AOD9604 reduced body-weight gain and increased fat oxidation and lipolysis in obese mice. Unlike intact hGH in this model, it did not bind the hGH receptor or induce hGH-receptor-mediated cell proliferation.

Cibinetide increased corneal and cutaneous small-nerve-fiber abundance in patients with sarcoidosis-associated small-fiber loss. The findings support biological activity but do not constitute approval.

In type 2 diabetes with painful neuropathy, ARA-290 was associated with improvement in neuropathic symptoms and selected metabolic measures over a short trial. No major safety issue was identified, but larger confirmatory studies were required.

In patients with sarcoidosis-associated small-fiber neuropathy, 28 days of ARA-290 improved neuropathic symptoms and was associated with increased corneal nerve-fiber density. The trial was small and exploratory.

PubChem's Cibinetide compound record establishes the identity of the 11-amino-acid synthetic peptide derived from the three-dimensional structure of erythropoietin. Used for identity verification only, not efficacy evidence.

On July 23, 2026, the FDA Pharmacy Compounding Advisory Committee voted 8-6 with one abstention to recommend possible 503A-list inclusion for BPC-157. The vote was advisory and nonbinding and did not create FDA approval, establish safety or effectiveness, or authorize a consumer product.

A registered 2026 trial is designed to investigate BPC-157 for acute grade-II hamstring injury. Registration or recruitment status does not establish safety or effectiveness and should not be reported as a positive result.

A 2026 review of BPC-157 musculoskeletal evidence found that human clinical evidence remains limited to small, uncontrolled, or retrospective reports and does not establish that BPC-157 heals tendons, ligaments, muscle, or cartilage in humans.

A 2026 review of BPC-157 translational development barriers found that much of the historical preclinical literature originates from a limited investigator network, and that formulation, replication, and translation to human trials remain significant unresolved barriers.

MitoCore-performed literature search (PubMed/PMC) for adequate human clinical trial or controlled human-outcome data for Bronchogen (AEDL), Testagen (KEDG), Chonluten (EDG), Prostamax (KEDP), and Ovagen (EDL). For each of these five subjects, the complete indexed source set located in the Batch 9 research pass and reconciliation is limited to cell, tissue, animal, or review-level sources -- no randomized, controlled, or otherwise adequate human clinical trial was located for any of the five. This is a MitoCore editorial search-audit record documenting an absence result across the existing source set for these five subjects; it is not itself a clinical trial, primary study, or regulatory approval document.

Reports DNA thermal-stability effects of Bronchogen. NOTE: this paper's own title states the sequence as Ala-Asp-Glu-Leu, an outlier versus later papers in the same lineage which converge on Ala-Glu-Asp-Leu (AEDL) -- retained here as a documented source inconsistency, not the canonical sequence.

A cross-species short-peptide gene-expression screen in tobacco (Nicotiana tabacum) plants that includes the AEDL/Bronchogen sequence. Useful only for sequence-naming corroboration -- this is a PLANT gene-expression study, not human or mammalian biology, and must not be cited as biological/mechanistic support for a human respiratory claim.

Novo Nordisk states that cagrilintide monotherapy is being advanced in the RENEW phase 3 program and cites REDEFINE 1 monotherapy data. This supports late-stage investigational status as of the research date, not approval.

Confirms a New Drug Application for CagriSema (cagrilintide + semaglutide) was submitted to the FDA in December 2025; decision expected in 2026. Cagrilintide is not FDA-approved as a standalone product.

An early controlled Phase 1b study reported greater weight reduction with co-administered cagrilintide and semaglutide than with comparator arms in selected adults, including people with type 2 diabetes. Findings describe the combination and must not be attributed to cagrilintide monotherapy.

Covers cagrilintide's chemical development. Full text was paywalled (403) beyond title/journal/DOI verification — do not cite specific findings from this source beyond that it exists and covers chemical development.

FDA's Global Substance Registration System identifies cagrilintide (UNII AO43BIF1U8) as an amylin-analogue peptide substance. A UNII record establishes chemical/substance identity only and does not indicate FDA approval, safety review, or effectiveness determination.

REDEFINE 2, a Phase 3a trial in adults with obesity and type 2 diabetes, reported significantly greater weight reduction with cagrilintide-semaglutide (CagriSema) than placebo in that population. The result applies to the exact combination product, escalation scheme, population, and duration studied -- not to cagrilintide monotherapy.

Official ClinicalTrials.gov registry record for REDEFINE 3, the dedicated cardiovascular-outcomes trial for cagrilintide-semaglutide. Cardiovascular-event-reduction benefit is not yet established pending this trial's results.

A laboratory study of AEDR/Cardiogen reported altered expression of cytoskeletal and nuclear-matrix proteins. These molecular findings do not establish organ specificity, clinical target engagement, or therapeutic benefit.

A U.S. patent describes AEDR/Cardiogen as a peptide substance related to myocardial function. Patents are intellectual-property documents, not clinical validation of safety or efficacy, and are retained here for identity/history context only.

The updated Cochrane review found no clear mortality benefit and continuing uncertainty for important clinical outcomes. It provides a conservative evidence boundary against overgeneralizing positive individual trials.

A 2020 FDA warning letter stated that a pharmacy's compounded Cerebrolysin products were not components of FDA-approved human drugs, were not supported by an applicable USP/NF monograph, and were not on the 503A Bulks List at that time. The letter also documented serious sterile-production deficiencies at that facility. This does not establish that every foreign authorized finished product is adulterated -- it establishes that the cited compounded U.S. products were ineligible for 503A exemptions and lacked FDA approval.

In a 192-participant randomized trial, the global CIBIC+ measure favored Cerebrolysin at week 12; the abstract did not report a significant ADAS-Cog treatment difference; baseline imbalances were present; adverse events were common in both groups.

Some randomized studies report improvements in cognition and global function in mild-to-moderate vascular dementia. Evidence quality, replication, and applicability to modern diagnostic criteria remain limitations.

The CAPTAIN program reports signals of improved multidimensional recovery after moderate-to-severe TBI. The evidence does not establish routine use in all TBI, benefit after remote concussion, healthy cognitive enhancement, prevention of chronic traumatic encephalopathy, or a self-directed recovery protocol.

A randomized study combining Cerebrolysin with alteplase found the combination was tolerable but did not improve the principal day-90 outcome. Short-term neurological measures favored treatment during the exposure period.

Cerebrolysin has foreign prescribing information for selected cerebrovascular, dementia, and brain-injury indications, including hypersensitivity, epilepsy, and severe-renal-impairment contraindications/cautions. Foreign authorization does not create U.S. FDA approval. Used for identity and foreign-label context only.

FDA distinguished CJC-1295 free-base/acetate from DAC forms, documented inconsistent nomenclature, found that none are components of FDA-approved drugs, and concluded that the available criteria weighed against placement on the 503A Bulks List.

At the December 4, 2024 meeting, CJC-1295 DAC free base, CJC-1295 DAC acetate, and CJC-1295 DAC trifluoroacetate each received 0 votes for inclusion and 13 votes against inclusion on the 503A Bulks List.

FDA’s briefing evaluation concluded that the criteria weighed against placing the evaluated CJC-1295 free-base, acetate, DAC, DAC-acetate, and DAC-TFA substances on the 503A Bulks List. The advisory committee’s recommendation is non-binding and is not itself an approval or final enforcement decision.

Human randomized trials showed prolonged GH and IGF-I increases after the long-acting DAC-containing CJC-1295 development compound. FDA specifically notes these clinical references concern CJC-1295 DAC, so they must not be used as direct human efficacy evidence for CJC-1295 free base/no-DAC.

The study identified a long-acting albumin-binding CJC-1295 conjugate and characterized prolonged activity. Because the paper concerns the albumin bioconjugate, it belongs with the DAC form rather than the non-DAC page.

An in-vitro study reported that Cortagen/AEDP altered IL-2 mRNA gene expression in mouse splenocytes. This molecular finding does not establish a validated human immune target, clinical immune benefit, or tissue specificity.

An in-vitro stem-cell study reported effects of short peptides, including AEDP, on neuronal differentiation of human periodontal stem cells. This cell finding does not establish human neurogenesis, cognitive benefit, or clinical tissue specificity.

Animal and tissue studies from the same research lineage reported effects of Crystagen on markers associated with B-cell immunity and age-related spleen changes; one study reported activation of B-cell-related immunity but no improvement in cellular-renewal processes in the aging spleen. These findings are preclinical, limited, and not independently replicated across multiple research groups.

A 2011 laboratory study evaluated short tripeptides in primary embryonic mesenchymal cells, fibroblasts, human K-562 erythromyelosis cells, and lymphoid-cell systems, reporting differential effects on proliferation, including stimulation of spontaneous proliferation in normal lymphocytes and inhibitory effects in selected embryonic or immortalized cell systems. This was cell-based research; it does not establish immune restoration, infection prevention, cancer treatment, or clinical safety.

A small human study reported endocrine effects of intravenous dermorphin exposure, including changes in prolactin, growth hormone, renin, and ACTH/cortisol. This is small, old, route-specific human pharmacology, not evidence of a modern approved therapeutic use.

A clinical-history review discusses older intrathecal postoperative and cancer-pain findings for dermorphin. The review frames these as historical small studies, not evidence of a modern approved analgesic, superiority to morphine, reduced addiction potential, or a safe consumer protocol.

A review of the dermorphin peptide family describes dermorphin as the amidated heptapeptide Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2, a potent mu-opioid receptor agonist originally isolated from Phyllomedusa frog skin, and situates it among a distinct family that includes deltorphins and dermenkephalin -- related but chemically and pharmacologically separate peptides that must not be merged with dermorphin itself.

WADA's 2026 Monitoring Program lists dermorphin and analogues among narcotics monitored in competition. Monitoring status is explicitly NOT the same as inclusion on the WADA Prohibited List and must not be described as prohibition.

Dihexa has been studied in zebrafish hair-cell injury and other laboratory systems. Protective effects were model-, toxin-, dose-, and pathway-specific and were not universal; preclinical c-Met activation must not be generalized into brain repair, hearing restoration, motor-neuron repair, or tissue regeneration.

In neuronal systems, Dihexa was associated with dendritic spine formation, synaptogenesis, and increased miniature excitatory postsynaptic current frequency, with effects blocked by HGF antagonism or c-Met suppression. These findings support an experimental HGF/c-Met-dependent mechanism and do not establish safe or beneficial human neurogenesis.

Orally administered Dihexa improved performance in the APP/PS1 Alzheimer-model mouse, a model-specific finding that does not establish treatment of Alzheimer disease, mild cognitive impairment, traumatic brain injury, Parkinson disease, or healthy aging.

FDA announced that Dihexa acetate is among substances intended for discussion by the Pharmacy Compounding Advisory Committee for possible 503A-list inclusion. Advisory review or nomination is not FDA approval, and no final favorable FDA determination was identified as of the research cutoff.

FDA states that it has not identified human exposure data for drug products containing Dihexa acetate administered by any route and lacks important information needed to determine whether it would harm humans.

Dihexa is a metabolically stabilized Angiotensin-IV-derived analogue distinct from native Angiotensin IV and Nle1-Angiotensin IV. Laboratory studies report that Dihexa binds HGF and potentiates HGF-dependent c-Met activation.

Dihexa, also called PNB-0408, is the metabolically stabilized Angiotensin-IV-derived analogue N-hexanoic-Tyr-Ile-(6-aminohexanoic amide) -- a small peptidomimetic/oligopeptide-derived molecule rather than a native endogenous peptide, distinct from Angiotensin IV, HGF, c-Met, HGF/c-Met agonist antibodies, fosgonimeton, and other unrelated compounds.

Recent structural work further characterized the interaction of FOXO4 and FOXO4-DRI with the disordered p53 transactivation domain. Mechanistic clarification does not establish therapeutic selectivity or human safety.

Mouse and cell studies reported reduced senescent Leydig-cell burden, improved testicular microenvironment, and partial restoration of age-related testosterone secretion in mice. These findings do not establish treatment of human hypogonadism, infertility, low testosterone, erectile dysfunction, or age-related reproductive decline.

The 2017 Cell study identified FOXO4 as a regulator of senescent-cell viability and developed FOXO4-DRI to compete with FOXO4-p53 binding. In cultured senescent cells, the peptide promoted p53 redistribution and apoptosis. In progeroid and naturally aged mice, treatment was associated with improvements in selected measures including activity, fur density, and renal-function markers. These results were preclinical and did not demonstrate increased human lifespan, reversal of human aging, or clinical safety.

A Phase 2 randomized, double-blind, vehicle-controlled split-wound study of topical GHK-Cu gel in healthy adults began in 2026 and was recruiting as of the research cutoff. No results were posted. Trial registration is not evidence of safety or effectiveness.

A multicenter, randomized, evaluator-blinded, vehicle-controlled study of a topical glycyl-L-histidyl-L-lysine:copper complex gel alongside standardized wound care reported greater closure of diabetic neuropathic plantar ulcers and fewer infections than vehicle. The evidence is old, concerns a specific topical gel and standardized wound-care protocol, and does not establish injectable efficacy or generalized healing of tendons, ligaments, muscle, joints, nerves, or surgical wounds.

As of the May 14, 2026 list, GHRP-2 and GHRP-6 are both Category 1 substances under FDA evaluation for the 503A Bulks List. Category 1 status is not FDA approval and does not establish a finding of safety or effectiveness or automatic authorization to compound.

Failed to reverse growth hormone deficiency and did not stimulate growth; the increase in body weight observed reflected worsened body composition, not benefit. Included here as a negative result to avoid cherry-picking only positive studies.

PubChem identity record for pralmorelin (GHRP-2), a synthetic six-residue growth-hormone-releasing peptide containing non-natural amino-acid residues and acting primarily at the ghrelin/growth-hormone-secretagogue receptor.

PubChem identity record for GHRP-6, a synthetic six-amino-acid growth-hormone-releasing peptide containing non-natural D-amino-acid residues and acting as a ghrelin/growth-hormone-secretagogue-receptor agonist.

Reduced myocardial collagen I/III deposition; the effect was blocked by a GHS-R antagonist, indicating a GHS-R-dependent fibrosis pathway distinct from the GH-independent CD36 pathway (both mechanisms are real and coexist).

Ejection fraction increased in ischemic cardiomyopathy patients but not dilated cardiomyopathy patients, despite similar GH release in both groups — suggesting direct myocardial stimulation distinct from GH release.

PubChem identity record for hexarelin (examorelin), a synthetic six-amino-acid peptidyl growth-hormone secretagogue and ghrelin-receptor agonist, a modified GHRP-family compound containing non-natural amino-acid residues.

FDA's Pharmacy Compounding Advisory Committee briefing on CJC-1295-related bulk drug substances also documented marketplace products combining growth-hormone-fragment materials with other compounded peptides. This regulatory context does not establish an FDA-sanctioned combination product or human efficacy/safety for HGH Fragment 176-191.

A 2022 study evaluated hGH Fragment 176-191 as part of a chitosan-nanoparticle formulation combined with doxorubicin against MCF-7 breast-cancer cells. This was an in-vitro drug-delivery experiment; it did not administer the peptide to humans and does not establish cancer treatment, fat loss, metabolic benefit, systemic safety, standalone peptide efficacy, or efficacy of ordinary lyophilized marketplace material.

WADA-sponsored analytical work has documented mislabeled performance-enhancing peptide products, including a vial labeled HGH Frag 176-191 that contained a different peptide. This illustrates product-identity risk rather than the safety of authentic material.

Highly purified hMG and recombinant FSH produced broadly comparable efficacy in this selected ART population; differences in selected adverse and pregnancy outcomes were exploratory and regimen-specific.

FDA's May 2026 evaluation of KPV free base and acetate for the 503A Bulks List found inadequate physicochemical and quality characterization, inconsistent naming, no identified human administration data, no clinical evidence for wound healing or inflammatory conditions, no human pharmacokinetic or pharmacodynamic studies, insufficient clinical and nonclinical safety information, and unresolved immunogenicity and aggregation concerns.

Victoza is indicated as an adjunct to diet and exercise to improve glycemic control in adults and pediatric patients aged 10 years and older with type 2 diabetes, and to reduce major adverse cardiovascular events in adults with type 2 diabetes and established cardiovascular disease. Saxenda's weight-management indication must not be transferred to Victoza, nor Victoza's diabetes/cardiovascular indication to Saxenda.

3,731 adults without diabetes were randomized to liraglutide 3.0 mg or placebo with lifestyle intervention for 56 weeks. Mean weight loss was approximately 8.4 kg with liraglutide versus 2.8 kg with placebo; more liraglutide-treated participants achieved at least 5% and more than 10% weight loss. These are group averages under a controlled trial and do not guarantee individual results.

This work demonstrates that LL-37 can participate in inflammatory/pathologic signaling in an Alzheimer's-disease model context, underscoring that LL-37 is immunologically active rather than a uniformly beneficial antimicrobial peptide. It does not establish clinical toxicity from therapeutic LL-37 use.

FDA has announced that cathelicidin LL-37 is intended for future Pharmacy Compounding Advisory Committee discussion. No meeting date, advisory vote, final listing decision, or favorable FDA action was identified as of the research cutoff (2026-07-30). A future advisory review is not approval and does not establish compounding eligibility.

LL-37 can form complexes with self-RNA that stimulate innate immune signaling, contributing to inflammatory and autoimmune biology rather than acting as a simple immune enhancer. This is a distinct source record from the dataset's existing self-DNA (PMID 17873860) and self-RNA/TLR7-8 (PMID 19703986) studies, which carry different PMIDs.

LL-37 is recognized as a T-cell autoantigen in psoriasis, implicating it in autoimmune pathophysiology and contradicting simplistic claims that more LL-37 is always beneficial. Distinct source record from the dataset's existing PMID 21850017 (keratinocyte/TLR9 reactivity) study.

In cultured cells, IGF-binding-protein-3 suppressed native IGF-I-stimulated proliferation more than Long R3 IGF-I-stimulated proliferation, consistent with Long R3 IGF-I's reduced IGFBP affinity. Cell-culture potency differences do not establish human efficacy, tissue selectivity, or safety.

The original engineering paper describes a family of related IGF-I muteins -- including Long IGF-I (N-terminal extension only), R3-IGF-I (Arg3 substitution only), Long R3 IGF-I (both modifications), and Long R3A16 IGF-I (an additional mutation) -- with differing IGF-binding-protein affinity and receptor potency. These related but distinct muteins must not be merged with one another or with native IGF-I.

Structural analysis confirms the Arg3 substitution and 13-amino-acid N-terminal extension defining Long R3 IGF-I, and describes altered N-terminal conformation alongside preserved IGF-domain structure. This establishes molecular identity, not therapeutic benefit.

WADA-funded research specifically addresses analytical detection of IGF-I and Long R3 IGF-I in anti-doping testing. This is anti-doping analytical methodology, not a human administration, efficacy, or safety study.

FDA's May 14, 2026 503A bulk drug substance category document places Mechano Growth Factor in Category 3, meaning it was nominated without adequate support. Category 3 is not FDA approval, is not inclusion on the 503A Bulks List, is not Category 1 status, and does not establish compounding eligibility, safety, or effectiveness.

A review of E-domain/MGF biological activity discusses proposed IGF-I-receptor-independent signaling and tissue-repair roles while noting that an autonomous circulating 24-amino-acid E-domain peptide has not been definitively isolated from human tissues or biological fluids. Transcript-level and full-length-protein evidence cannot be assumed to establish this.

FDA describes safety risks associated with certain compounded bulk drug substances, including identity, purity, and quality uncertainty. PEG-MGF has separate FDA safety concerns documented elsewhere and must not be merged into this page's MGF discussion.

Describes laboratory expression of full-length recombinant human MGF/pro-IGF-1Ec in E. coli. Full-length recombinant-protein evidence cannot be assigned to the 24-amino-acid synthetic E-domain peptide or to marketplace products of uncertain sequence and purity.

A synthetic MGF-Ct24E E-domain peptide promoted migration of human myogenic precursor cells in cell-based assays. This is a cell finding and does not establish human muscle hypertrophy, injury recovery, or disease treatment; independent replication attempts with MGF peptides found no apparent effect under different conditions.

Synthetic MGF E-peptide co-treatment improved engraftment of transplanted human myogenic precursor cells in a mouse model. This is a cell/animal transplantation finding, not a human treatment trial, and does not establish muscle repair or safety in humans.

A 2025 case report describes oral mucosal melanoma after Melanotan II nasal-spray use. As with other melanoma case reports for this compound, this cannot establish causation but is a safety signal that must remain visible, with uncertain product identity for the nasal-spray material used.

Analytical characterization of internet-sold Melanotan II products found problems involving content, purity, identity, and undeclared or inconsistent material. Human research material used in clinical studies cannot validate the identity, purity, sterility, or potency of an online product.

Case report of melanoma occurring during or after Melanotan II use. A case report cannot prove that Melanotan II caused the melanoma, given temporal association, confounding by UV/tanning-bed exposure, uncertain product identity, and incomplete surveillance data; it also does not support a claim that melanoma risk is absent.

Case report and review describing possible renal infarction associated with Melanotan II use, in addition to previously reported rhabdomyolysis and systemic toxicity. Case reports do not define incidence or prove causation but are clinically serious safety signals.

A review of unregulated alpha-MSH analogue use summarizes risks including microbial contamination, endotoxin, incorrect salt or concentration, degradation products, sterility failures, and mislabeled route or strength, in addition to the priapism, systemic toxicity, and pigmentary-lesion signals reported in individual case reports.

At the July 23-24, 2026 Pharmacy Compounding Advisory Committee meeting, FDA proposed that MOTS-c free base and MOTS-c acetate not be included on the 503A Bulks List, citing inadequate physical/chemical characterization, inconsistent naming and salt/derivative identity, lack of evidence supporting nominated uses, no identified human exposure data for drug products containing MOTS-c administered by any route, lack of clinical/nonclinical safety information, and unresolved immunogenicity risk. This is a proposal in the 503A review process, not a broader criminal-law or scheduling determination.

Observational study reporting associations between circulating MOTS-c and insulin sensitivity, glucose, HbA1c, obesity, and type 2 diabetes. Associations do not establish causation or treatment efficacy.

A direct search (PubMed, PMC, and general web) for "Ac-AEDG-NH2", "N-acetyl epitalon amide/amidate", "N-acetyl epithalon amide", and close spelling variants located no PubMed-indexed, PMC-indexed, clinical-trial, or clearly identifiable primary therapeutic study of the exact N-terminally acetylated, C-terminally amidated analogue. Only commercial synthesis/catalog pages, vendor product documentation, and pages extrapolating parent Epitalon/AEDG findings were located. A negative search does not prove no unpublished/non-indexed experiment exists; the correct wording is that no direct indexed study was identified in this research pass, not that no study exists anywhere.

2026 review of NAD+ anti-aging and wellness evidence. Human trials show NR and NMN can increase measured NAD-related metabolites under some conditions, but clinical outcome benefits are inconsistent; evidence for a precursor cannot be transferred automatically to direct NAD+ injection.

2026 retrospective real-world pilot: commercial NAD+ IV use remained poorly studied and reported tolerability problems during infusion. Authors called for adequately powered randomized placebo-controlled trials.

2025 randomized single-center study in ischemic cardiomyopathy: modest improvement in left-ventricular ejection fraction after seven days of low-dose IV NAD+ alongside standard therapy. Secondary clinical outcomes mostly nonsignificant trends. Requires independent replication; cannot support general heart-health or wellness claims.

FDA warned compounders that food-grade NAD+ is not suitable for sterile compounding without appropriate processing because of microbial and endotoxin risk. FDA received reports after NAD+ injectable products of severe chills, shaking, vomiting, and fatigue, with some patients requiring medical treatment; FDA stated these reactions were consistent with excessive endotoxin levels.

Neither Orexin A nor Orexin B was identified as a current individually evaluated substance in the reviewed FDA 503A bulk-substance category list or FDA significant-safety-risk table as of this update. Absence from those lists is not approval, a safety determination, or authorization to compound.

FDA Office of Orphan Products Development (OOPD) record (grid key 1121625) lists an orphan-drug designation for oveporexton (sponsor: Takeda Pharmaceuticals U.S.A., Inc.), designated March 2, 2026, for the orphan designation "treatment of narcolepsy type 1 (narcolepsy with cataplexy)." Status: Designated. FDA orphan approval status: Not FDA Approved for Orphan Indication. Orphan designation is not marketing approval. This record concerns oveporexton, not native Orexin A.

On February 10, 2026, the FDA accepted Takeda's New Drug Application and granted Priority Review for oveporexton (TAK-861), an investigational oral OX2R-selective small-molecule orexin receptor agonist, for narcolepsy type 1. The FDA assigned a PDUFA target action date in the third quarter of 2026. Oveporexton is not Orexin A and was not FDA approved as of this review date (July 14, 2026); its NDA is supported by the phase 3 FirstLight and RadiantLight trials, which evaluated oveporexton, not native Orexin A.

This systematic review identified three eligible human Orexin A studies. The evidence suggested changes in REM-sleep measures (decreased wake-REM transitions and total REM sleep time) but did not establish increased wake time or support routine replacement therapy. The review's own authors concluded orexin deficiency is not the only factor in narcolepsy type 1 pathophysiology. This review does not override or add evidentiary weight beyond what its three small underlying primary studies individually support, and the underlying human evidence base for Orexin A remains small.

Intranasal orexin A significantly increased resting muscle sympathetic nerve activity (MSNA) burst rate versus placebo (+5.8 ± 0.8 vs +2.1 ± 0.6 bursts/min, P = 0.007) in a small double-blind crossover pilot study of 10 healthy men. Blood pressure, heart rate, heart-rate variability, and baroreflex sensitivity were not acutely altered.

In a double-blind, randomized, placebo-controlled crossover trial, seven patients with narcolepsy and cataplexy showed improved olfactory threshold scores after intranasal Orexin A (hypocretin-1) compared with placebo. This is a very small study and does not establish general treatment efficacy, improved wakefulness, long-term benefit, or routine use, and the olfactory finding must not be generalized to other symptoms or populations.

Orexin A activates both OX1R and OX2R with high functional activity at each. Orexin B activates OX2R efficiently but has substantially weaker functional activity at OX1R than Orexin A, so the two peptides must not be treated as interchangeable or dose-equivalent.

Danavorexton is a synthetic, nonpeptide OX2R agonist studied in humans. It is a distinct molecular class from native Orexin A/Orexin B. Results from danavorexton, oveporexton, or another synthetic receptor agonist cannot establish the identity, stability, brain penetration, dosing, safety, or effectiveness of native orexin peptide products -- used here only as an identity/evidence boundary, not as orexin-peptide evidence.

Animal studies report Orexin A effects on wakefulness and cognitive performance during sleep deprivation. This nonhuman-primate finding does not establish human treatment of fatigue, cognitive impairment, obesity, depression, ADHD, dementia, sleep deprivation, or athletic performance.

Cell and receptor-signaling research supports OX2R-mediated arousal signaling, receptor signaling and desensitization. These findings remain preclinical/cellular and do not establish human administered-Orexin-B efficacy or safety.

Orexin B, also called hypocretin-2, is an endogenous linear 28-amino-acid neuropeptide generated from prepro-orexin. The mature human peptide is C-terminally amidated. Human and rodent Orexin B sequences are not identical; species-specific sequence must be verified.

Structure-activity relationships for Orexin A and Orexin B are concentrated in the C-terminal region. Orexin B is often described as relatively OX2-preferring, but it is not an absolutely selective OX2R ligand, and results from a synthetic selective OX2R agonist cannot be assigned to native Orexin B.

Full-text version of the direct 2017 PE-22-28 research program: inhibition of human TREK-1 current in transfected cells with apparent potency exceeding parent spadin, mouse forced-swim/learned-helplessness/corticosterone/novelty-suppressed-feeding findings, increased BrdU-positive hippocampal cells after short mouse treatment, increased PSD-95 in cultured mouse cortical neurons, and longer measured activity than spadin in the tested mouse paradigm. All direct efficacy evidence remains preclinical and concentrated in one research group.

Reports parent-compound spadin effects on synaptogenesis. Kept as an explicit parent-compound boundary source: findings about spadin do not establish the same effect for the distinct, shorter PE-22-28 fragment.

Original discovery paper for spadin, the sortilin-derived parent peptide from which PE-22-28 (residues 22-28) is fragmented, targeting rodent TREK-1 channels. Parent-compound context: evidence about spadin itself cannot automatically be assigned to the shorter PE-22-28 fragment.

FDA states that compounded PEG-MGF may pose significant immunogenicity and impurity/API-characterization risks and that it has not identified human exposure data for PEG-MGF drug products. FDA also lists safety concerns for compounded Melanotan II.

A biophysical study examined EDR-DNA interaction using molecular-docking and structural methods. This supports a mechanistic hypothesis only, not a validated human receptor, pharmacodynamic biomarker, or disease-modifying mechanism.

A report involving locomotive workers described changes in biological-age and adaptation indicators after Pinealon use. The abstract does not provide the modern trial details needed to establish randomization, blinding, allocation concealment, validated clinical endpoints, complete adverse-event reporting, or durable benefit.

Laboratory studies reported that EDR/Pinealon reduced reactive-oxygen-species accumulation and necrotic cell death in selected neural and non-neural cell systems and altered ERK activation and cell-cycle behavior. These findings do not establish antioxidant therapy, neuroprotection, or clinical safety in humans, and cell-cycle effects create unresolved proliferative and oncologic questions.

Direct search performed 2026-08-17 for FDA drug-approval status and ClinicalTrials.gov interventional-trial registration for PNC-27, Pancragen, Bronchogen, Testagen, Chonluten, Prostamax, Ovagen, and N-Acetyl Epitalon Amidate (Ac-AEDG-NH2), including known aliases and sequence names. No FDA-approved drug product was identified for any of the eight compounds. No registered ClinicalTrials.gov interventional trial was identified for any of the eight compounds. All eight are marketed exclusively through peptide/research-chemical vendors as research-use-only products, not as approved medicines. Absence from these searches is not itself a formal FDA determination and does not establish safety or ineffectiveness -- it establishes only that no approval or registered trial was located in this search pass.

Experimental chronic aseptic prostatitis animal model reporting reduced inflammation signs and prevention of sclerotic/atrophic changes with Prostamax; preclinical, not a human controlled trial. Lower-tier journal; not independently replicated.

Explicitly identifies the studied oligopeptide as Lys-Glu-Asp-Pro (KEDP) and reports chromatin-organization effects in an aging model. Direct exact-sequence KEDP evidence, compatible with the Prostamax identity established by patent RU2177802C1.

Broader paper on epigenetic-regulator peptides in rodents with long and short lifespans; NOT an exact Prostamax/KEDP identity paper. Should not be used as a core exact-identity citation -- RU2177802C1 and PMID 23221144 are materially stronger for identity.

Patent explicitly claims the tetrapeptide Lys-Glu-Asp-Pro ("lysyl-glutamyl-aspartyl-proline"), lists Prostamax as the associated trade name, states it is prepared by classical peptide synthesis in solution, and explicitly distinguishes it from Prostatilen (a prostate-tissue-derived polypeptide preparation). Confirms Prostamax = synthetic KEDP, separate from tissue extracts.

FDA states retatrutide is not an FDA-approved drug and cannot be used in compounding under federal law because it is not a component of an FDA-approved drug and has not been found safe and effective for any condition.

TRIUMPH-Outcomes is designed to determine whether retatrutide reduces serious cardiovascular events and/or worsening kidney outcomes in adults with obesity and established atherosclerotic cardiovascular disease and/or chronic kidney disease; completed cardiovascular-outcome efficacy results are not yet available.

In a chronic social-stress rat model, Selank administration was associated with changes in circulating cytokines, including reductions toward control values for several pro-inflammatory mediators. Supports an immunomodulatory hypothesis but is not evidence of clinical anti-inflammatory efficacy.

Rat-brain membrane receptor-binding experiments found Selank altered radiolabeled GABA binding in a concentration-dependent manner and behaved as a positive allosteric modulator in experimental receptor-binding systems -- a mechanistic/analytical finding, not a human clinical mechanism.

In a rat unpredictable chronic mild stress model, Selank altered anxiety-related behavior and interacted with diazepam. A rodent behavioral-pharmacology finding, not evidence of human clinical anxiolytic efficacy.

A small comparative Russian study reported anxiolytic effects of Selank versus phenazepam in anxiety disorders. Limited by small sample size and older reporting standards; not independently replicated at multicenter scale.

A small older study, primarily from Russia, compared intranasal Selank with a benzodiazepine-type drug in patients described as having generalized anxiety disorder or neurasthenia and reported possible reductions in anxiety symptoms. Limited by small sample size, limited methodological detail, older diagnostic terminology, uncertain randomization/blinding, unclear formulation identity, short follow-up, and no FDA-reviewed efficacy program.

A small older Russian study examined Selank combined with phenazepam. Same limitations as the other small Selank studies: small samples, limited methodological detail, uncertain formulation identity, short follow-up, no independent replication, no FDA-reviewed efficacy program.

A small older Russian study compared intranasal Selank with phenazepam and described possible differences in sedation or cognition alongside anxiety-related effects. Same limitations as the other small Selank studies: small samples, limited methodological detail, uncertain formulation identity, short follow-up, no independent replication.

FDA approved NDA 215256 for Wegovy (semaglutide) injection on June 4, 2021, as an adjunct to a reduced-calorie diet and increased physical activity for chronic weight management in adults meeting the approved labeling criteria.