PT-141 — Research Overview
Chemical Name: Bremelanotide; cyclic lactam heptapeptide melanocortin receptor agonist
Also Known As: PT-141, bremelanotide, Rekynda (EU investigational name)
Brand Name (FDA-Approved): Vyleesi (bremelanotide injection 1.75 mg/0.3 mL)
Structure: Synthetic cyclic heptapeptide — a structural analog of alpha-melanocyte-stimulating hormone (alpha-MSH). Contains the His-Phe-Arg-Trp core pharmacophore required for melanocortin receptor binding, presented within a cyclic lactam backbone that constrains the peptide’s three-dimensional conformation and provides resistance to enzymatic degradation.
Relationship to MT-2: PT-141 is a deaminated C-terminal metabolite of MT-2 (Melanotan II) — it shares the cyclic heptapeptide backbone of MT-2 but with structural modifications that shift receptor selectivity away from MC1R (the primary pigmentation receptor) toward MC3R and MC4R (the CNS receptors mediating sexual arousal and desire). This selective refinement was the key pharmacological advance that enabled PT-141’s clinical development: MT-2 produced both sexual arousal effects and skin darkening through MC1R; PT-141 substantially retains the sexual arousal profile while reducing the melanogenic effect.
FDA Approval: June 21, 2019 (NDA 210557) — Vyleesi, for the treatment of acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women. Developed by Palatin Technologies; originally marketed by AMAG Pharmaceuticals.
Approved Indication: Acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women not due to a co-existing medical or psychiatric condition, problems within the relationship, or the effects of a medication or other drug substance.
Approved Dosing: 1.75 mg subcutaneous injection approximately 45 minutes before anticipated sexual activity. Maximum one dose per 24 hours, maximum 8 doses per month.
WADA Status: Not specifically prohibited as PT-141 by name on the WADA prohibited list as of this compilation; however, compounds affecting the melanocortin system may fall under related prohibited categories depending on context.
Regulatory Distinction: PT-141 is currently the only FDA-approved on-demand treatment for acquired, generalized HSDD in premenopausal women, and the first melanocortin receptor agonist approved as a systemic therapeutic for any sexual dysfunction indication. It is mechanistically distinct from all previously approved sexual dysfunction treatments by acting centrally in the brain rather than peripherally on genital vasculature.
Category: MC3R/MC4R melanocortin receptor agonist / centrally acting pro-sexual neuropeptide / FDA-approved pharmaceutical / dopaminergic desire circuit activator / research tool for melanocortin CNS pharmacology
Research Use Only — Disclaimer
The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption outside of the specific FDA-approved pharmaceutical indication described above (Vyleesi, HSDD in premenopausal women). The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.
What Is PT-141?
PT-141 is a synthetic cyclic heptapeptide and the pharmacologically refined descendant of MT-2 (Melanotan II), representing one of the clearest examples in modern drug development of how an unexpected serendipitous observation from a research compound is systematically translated into an approved medicine. The story begins with MT-2 tanning trials in the 1990s at the University of Arizona, where male subjects receiving MT-2 for its intended melanogenic effects reported an entirely unexpected adverse event: spontaneous penile erections occurring 1 to 5 hours after injection. Rather than dismissing this observation, the research team recognized its profound therapeutic significance — that central melanocortin receptor activation through an entirely novel pathway could produce sexual arousal independent of the peripheral vascular mechanisms targeted by all existing erectile dysfunction treatments.
The subsequent controlled clinical studies of MT-2 in men with psychogenic and organic erectile dysfunction by Wessells and colleagues directly established the proof-of-concept that subcutaneous melanocortin agonist administration produces clinically meaningful erectogenic effects through central MC4R-mediated pathways. These studies demonstrated that erections occurred without sexual stimulation, distinguishing the melanocortin mechanism from PDE5 inhibitors (which require sexual stimulation and intact vascular function) and identifying central desire-initiating rather than peripheral arousal-facilitating mechanisms as the pharmacological basis.
PT-141 (bremelanotide) was developed as a structurally refined analog of MT-2 specifically designed to preserve the MC3R/MC4R-mediated sexual arousal activity while reducing MC1R-mediated melanogenic (skin-darkening) effects that were a clinically problematic feature of MT-2. This receptor selectivity engineering — shifting toward CNS-relevant receptors and away from skin pigmentation — was the key pharmacological innovation enabling clinical development. Through an extensive Phase 2 and Phase 3 clinical program in both male and female populations, bremelanotide was ultimately approved by the FDA in June 2019 as Vyleesi — the first and currently only on-demand FDA-approved treatment for acquired, generalized HSDD in premenopausal women, and the first melanocortin receptor agonist approved for sexual dysfunction treatment.
Hypoactive Sexual Desire Disorder — The Approved Indication
Hypoactive sexual desire disorder (HSDD) is the most prevalent female sexual dysfunction, affecting an estimated 10% of women aged 18 to 44 years in the United States and characterized by persistently diminished or absent desire for sexual activity accompanied by personal distress or interpersonal difficulty. The distress component is diagnostically essential — low sexual desire that does not cause personal distress does not meet the HSDD diagnostic threshold.
HSDD represents a significant unmet medical need: prior to bremelanotide’s approval, only one FDA-approved treatment existed for female sexual desire dysfunction (flibanserin/Addyi, approved 2015 for daily oral use in premenopausal women with HSDD), and no on-demand treatment option was available. Bremelanotide filled this gap as an as-needed treatment — taken only when sexual activity is anticipated, rather than requiring daily adherence.
The pathophysiology of HSDD involves disruption of the central neural systems that generate sexual motivation and desire. These systems include the hypothalamic-limbic dopamine circuits (the mesolimbic reward pathway projecting from the ventral tegmental area to the nucleus accumbens), melanocortin circuits in the paraventricular nucleus of the hypothalamus, and oxytocin pathways modulated by these circuits. Bremelanotide’s mechanism — direct MC3R/MC4R activation in these hypothalamic regions — pharmacologically amplifies the neural circuits responsible for desire initiation, acting upstream of the stimulus-response pathway that conventional treatments attempt to optimize downstream.
Mechanism of Action
MC3R and MC4R agonism — the central desire circuit: PT-141 binds and activates MC3R and MC4R in the brain, particularly in the paraventricular nucleus (PVN) of the hypothalamus, the ventromedial hypothalamus, and connected limbic regions that together constitute the brain’s sexual motivation circuitry. Both receptor subtypes contribute to the pro-sexual effect, with MC4R appearing to be the primary effector. This receptor binding is through Gs-coupled adenylyl cyclase activation and cAMP elevation — the same intracellular signaling pathway used by melanocortin receptors throughout the body.
Dopamine release amplification: MC4R activation in hypothalamic neurons that project to the mesolimbic dopamine system facilitates presynaptic dopamine release in reward pathway terminals. This dopaminergic amplification is a central mechanism by which bremelanotide enhances subjective desire. The mesolimbic dopamine system — projecting from the ventral tegmental area (VTA) through the nucleus accumbens to the prefrontal cortex — is the neurobiological substrate of wanting, motivation, and anticipatory reward. Pharmacological activation of this circuit through MC4R → dopamine represents amplification of the neurochemical signal that the brain interprets as sexual wanting. This mechanism explains why bremelanotide can generate desire in the absence of external sexual stimuli — it is acting upstream of the stimulus-response pathway, directly enhancing the internal motivation signal.
Oxytocin pathway engagement: MC4R activation in the PVN also stimulates oxytocin release from PVN neurons that project throughout the brain. Oxytocin contributes to pro-sexual CNS effects including facilitation of sexual receptivity, enhancement of social bonding, and potentiation of genital sensitivity. This oxytocin dimension adds a social and affiliative dimension to bremelanotide’s pro-sexual mechanism beyond simple dopaminergic desire activation.
Central-to-peripheral nitric oxide cascade: MC4R activation in the hypothalamus and lumbosacral spinal cord initiates a descending neural signal that ultimately triggers nitric oxide (NO) release from nitrergic neurons innervating genital tissue. This NO-mediated genital vasodilation and smooth muscle relaxation produces the physical arousal response — genital engorgement in both sexes. The critical pharmacological distinction from PDE5 inhibitors is the origin of this NO signal: bremelanotide’s NO originates from a central neurological command initiated by hypothalamic MC4R activation, whereas PDE5 inhibitors prevent degradation of locally produced NO already present in genital smooth muscle in response to sexual stimulation. Bremelanotide does not require sexual stimulation to initiate the genital arousal response; PDE5 inhibitors do.
Reduced MC1R activation compared to MT-2: The structural modifications in PT-141 relative to MT-2 substantially reduce activity at MC1R — the primary receptor driving melanocyte activation and skin darkening. This selectivity shift reduces the melanogenic side effects (tanning, hyperpigmentation, mole darkening) that characterized MT-2 and limited its clinical development. PT-141 still has some MC1R activity, which explains the transient skin flushing and mild facial pigmentation changes reported in some subjects, but the magnitude of these effects is substantially reduced compared to MT-2.
The Developmental Timeline — From MT-2 Adverse Event to FDA Approval
1984: Dorr et al. Phase 1 tanning trials of MT-2 at University of Arizona — spontaneous erections first observed as unexpected adverse event.
1998: Wessells et al., Journal of Urology — first controlled double-blind study of MT-2 in psychogenic erectile dysfunction: 8/10 subjects developed erections, mean duration 38 minutes, versus 3 minutes placebo.
2000: Wessells et al., Urology — MT-2 in organic erectile dysfunction: erections in 12/19 drug injections versus 1/21 placebo injections.
Early 2000s: Development of PT-141 (bremelanotide) as refined MT-2 analog with improved receptor selectivity. Initial development by Palatin Technologies.
2003-2004: Phase 1 and Phase 2 intranasal PT-141 studies in men — produced statistically significant erectile activity by RigiScan; identified as first CNS-acting pro-erectile agent.
2006: Phase 2 study in premenopausal women with HSDD — bremelanotide (intranasal) showed significant improvements in desire and subjective arousal. First controlled evidence for efficacy in female sexual dysfunction.
2008: Intranasal formulation program halted after blood pressure concerns identified in Phase 2b. Reformulation to subcutaneous injection.
2014-2016: Phase 2b dose-finding trial in premenopausal women with HSDD — established optimal 1.75 mg subcutaneous dose.
2015-2016: RECONNECT Phase 3 trials (Studies 301 and 302) enrollment.
June 21, 2019: FDA approval of bremelanotide injection (Vyleesi, 1.75 mg) for acquired, generalized HSDD in premenopausal women.
Published Research
Study 1 — MT-2 Proof of Concept: Synthetic Melanotropic Peptide Initiates Erections in Psychogenic Erectile Dysfunction
Authors: Wessells H, Fuciarelli K, Hansen J, Hadley ME, Hruby VJ, Dorr R, Levine N
Year: 1998
Journal: Journal of Urology
PMID: 9679884
This double-blind placebo-controlled crossover study in 10 men with psychogenic erectile dysfunction was the foundational clinical proof-of-concept from which PT-141’s entire development descended — the first controlled human demonstration that MC4R agonism produces clinically significant erections through a central, non-vascular mechanism.
Eight of 10 MT-2-treated subjects developed clinically significant erections with greater than 80% rigidity measured by RigiScan. Mean duration was 38 minutes with MT-2 versus 3 minutes with placebo (P equal to 0.0045). Erections occurred spontaneously — without sexual stimulation — confirming central rather than peripheral origin.
Side effects (nausea, stretching, yawning, appetite suppression) were dose-dependent and mild at the preferred 0.025 mg/kg dose — establishing the tolerability foundation for subsequent development.
This study’s conclusion that MT-2 safely initiates erections through central melanocortinergic mechanisms was the scientific catalyst for PT-141 development, redirecting melanocortin research from tanning toward sexual dysfunction therapeutics.
Study 2 — Phase 2 in Men with Organic Erectile Dysfunction: Erectogenic Properties Extend Beyond Psychogenic ED
Authors: Wessells H, Gralnek D, Dorr R, Hruby VJ, Hadley ME, Levine N
Year: 2000
Journal: Urology
PMID: 11018622
This controlled study extended MT-2 investigation to men with organic erectile dysfunction risk factors — a more clinically relevant and challenging population — and characterized sexual desire effects alongside erectogenic properties.
Erections were reported following 12 of 19 MT-2 injections versus only 1 of 21 placebo injections across 10 men with average 2.2 organic ED risk factors. Mean RigiScan tip rigidity duration was 45 minutes versus 2 minutes for placebo.
Increased sexual desire was reported following 10 of the drug injections — the first controlled human evidence that central melanocortin receptor agonism increases desire, not merely physical erection. This desire-enhancing observation was the critical finding that redirected development toward female HSDD, where the primary pathology is desire impairment rather than vascular dysfunction.
The conclusion — that erectogenic effects are not limited to psychogenic ED and that increased desire warrants further investigation of centrally-acting melanocortin agents — directly shaped the clinical development strategy toward what became the FDA-approved HSDD indication.
Study 3 — Phase 2b Dose-Finding: Bremelanotide in Premenopausal Women with HSDD
Authors: Clayton AH, Althof SE, Kingsberg S, DeRogatis LR, Kroll R, Goldstein I, Kaminetsky J, Spana C, Lucas J, Jordan R, Portman DJ
Year: 2016
Journal: Women’s Health (London)
PMID: 27181790
This Phase 2b randomized placebo-controlled dose-finding trial in premenopausal women established the efficacy of subcutaneous bremelanotide for female sexual dysfunction across multiple endpoints and identified the optimal dose for Phase 3 development.
327 subjects in the modified intent-to-treat population provided efficacy data. For the pooled 1.25/1.75 mg dose group versus placebo, mean changes from baseline included 0.7 versus 0.2 satisfying sexual events per month (P equal to 0.0180), 3.6 versus 1.9 FSFI total score improvement (P equal to 0.0017), and -11.1 versus -6.8 reduction in FSDS-DAO total distress score (P equal to 0.0014).
These significant improvements across satisfying sexual events, overall sexual function, and sexual distress simultaneously — achieved with an as-needed subcutaneous injection — established the pharmacological basis for the Phase 3 RECONNECT program.
Adverse events were nausea, flushing, and headache — the same tolerability profile subsequently documented in Phase 3.
Study 4 — Phase 3 RECONNECT Trials: Definitive Evidence for HSDD Treatment in Premenopausal Women
Authors: Kingsberg SA, Clayton AH, Portman D, Williams LA, Krop J, Jordan R, Lucas J, Simon JA
Year: 2019
Journal: Obstetrics and Gynecology
PMID: 31599840
Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC6819021/
The RECONNECT studies were two identically designed parallel Phase 3 randomized double-blind placebo-controlled multicenter trials that constituted the primary FDA registration evidence for bremelanotide — enrolling 1,267 premenopausal women with acquired, generalized HSDD at sites across the United States and Canada.
Co-primary endpoints were the Female Sexual Function Index desire domain (FSFI-D) and the Female Sexual Distress Scale-Desire/Arousal/Orgasm (FSDS-DAO) item 13 (measuring distress from low desire), assessed over 24 weeks of as-needed bremelanotide 1.75 mg or placebo subcutaneous self-administration approximately 45 minutes before anticipated sexual activity.
From baseline to end of study, women taking bremelanotide showed statistically significant increases in sexual desire across both studies (Study 301: 0.30, P less than 0.001; Study 302: 0.42, P less than 0.001; integrated: 0.35, P less than 0.001) and statistically significant reductions in distress related to low sexual desire (Study 301: -0.37, P less than 0.001; Study 302: -0.29, P equal to 0.005; integrated: -0.33, P less than 0.001).
Cohen’s d effect sizes for the integrated population were 0.39 for improving sexual desire (FSFI-D) and 0.27 for decreasing related distress (FSDS-DAO Item 13) — in the small-to-medium range, similar to the effect size of once-daily flibanserin (0.29 to 0.44) in comparative analyses, and consistent with the modest but statistically significant effects characterizing the existing female sexual dysfunction treatment landscape.
A post hoc exploratory analysis showed the percentage of sexual encounters rated as satisfying sexual events increased more than two-fold in the bremelanotide group compared to placebo across both studies (25.0% versus 9.8%, P less than 0.001).
Treatment-emergent adverse events more frequent with bremelanotide included nausea (approximately 40% of subjects with first dose, diminishing with continued use), flushing (20-25%), and headache (12%). Most adverse events were mild to moderate in intensity. Transient blood pressure changes (3-6 mmHg mean decrease) occurred in some subjects, which is why a cardiovascular history contraindication is included in the prescribing information. No serious drug-related adverse events were reported in either study.
The authors concluded that both studies demonstrated bremelanotide significantly improved sexual desire and related distress in premenopausal women with HSDD, with a favorable safety profile — conclusions supported by the FDA in granting approval.
Study 5 — Long-Term Safety and Efficacy: 52-Week Open-Label Extension of RECONNECT
Authors: Simon JA, Kingsberg SA, Portman D, Williams LA, Krop J, Jordan R, Lucas J, Clayton AH
Year: 2019
Journal: Obstetrics and Gynecology
PMID: 31599847
This 52-week open-label extension of RECONNECT provided the long-term safety and sustained efficacy data that fully characterized bremelanotide’s profile over nearly a year of as-needed use.
Women who completed the 24-week core double-blind phase could enroll in the 52-week open-label extension. During this extended period, no new safety signals were observed — the same tolerability profile of nausea, flushing, and headache was maintained without emergence of new or more serious adverse events.
The most common treatment-emergent adverse events related to study drug during the extension were nausea (40.4%), flushing (20.6%), and headache (12.0%). Nausea was the only severe adverse event experienced by more than one participant, and even nausea’s frequency decreased with continued use — consistent with physiological accommodation.
Sustained efficacy was demonstrated: women who received bremelanotide during the core phase showed continued FSFI-D improvements of 1.25 to 1.30 from baseline by end of the open-label extension, and distress reductions of 1.4 to 1.7 — improvements that maintained or increased beyond those measured at the end of the 24-week blinded phase.
Women who received placebo during the core phase and switched to open-label bremelanotide showed FSFI-D improvements of 0.70 to 0.77, confirming that the active treatment effect was not a time-in-study artifact and that bremelanotide produces genuine pharmacological benefits when initiated.
PT-141 vs PDE5 Inhibitors — The Mechanistic Distinction That Defines the Indication
Understanding why PT-141 occupies a distinct pharmacological niche from sildenafil, tadalafil, and other PDE5 inhibitors is essential for accurate research context.
PDE5 inhibitors (sildenafil, tadalafil, vardenafil, avanafil) act peripherally: they block phosphodiesterase-5, the enzyme that degrades cyclic GMP in genital smooth muscle. By preventing cGMP degradation, they potentiate the vasodilatory response to nitric oxide released locally in genital tissue — but this NO is only released in response to sexual stimulation. PDE5 inhibitors therefore facilitate the physical arousal response once desire and stimulation are present, but do not address desire or arousal initiation. They are ineffective in individuals whose primary problem is absent desire, insufficient sexual motivation, or in whom the stimulation-to-NO pathway is damaged or absent.
PT-141 acts centrally: it activates MC3R and MC4R in the hypothalamus and limbic system, triggering dopamine release, oxytocin release, and descending neural signals that initiate the genital arousal response without requiring sexual stimulation as a prerequisite. PT-141 acts upstream of the stimulus-response pathway, at the desire-initiation level rather than the peripheral facilitation level.
This distinction creates clinically meaningful complementarity: PT-141 is relevant when desire and motivation are absent or impaired; PDE5 inhibitors are relevant when desire is intact but the peripheral vascular response is impaired. Combination research — PT-141 plus PDE5 inhibitors — has demonstrated additive effects in men with ED who do not fully respond to PDE5 inhibitor monotherapy, with the combination addressing both central desire and peripheral vascular response simultaneously.
Off-Label Research in Male Sexual Dysfunction
While FDA approval of PT-141 (Vyleesi) is specifically for premenopausal women with HSDD, bremelanotide has been studied in male erectile dysfunction and male hypoactive sexual desire, and off-label use in men through compounding pharmacies is increasingly common in clinical practice.
The foundational MT-2 studies in men with psychogenic and organic ED established proof of concept. Subsequent PT-141-specific Phase 2 studies using intranasal administration (before the reformulation to subcutaneous injection) demonstrated statistically significant erectile activity by RigiScan in men — including a study by Diamond et al. showing PT-141 produced erections in men who had not responded to sildenafil — providing evidence for the distinct and additive CNS mechanism relative to PDE5 inhibitors.
A randomized controlled trial by Safarinejad and Hosseini evaluated bremelanotide 10 mg intranasal spray in 342 men who failed to respond to sildenafil: approximately 34% of bremelanotide recipients responded to treatment compared to 8% of placebo recipients — though this study’s data were later subject to an expression of concern and results should be interpreted with additional caution alongside other evidence.
FDA approval was not pursued for male erectile dysfunction, as the development program was redirected to female HSDD where regulatory pathways were clearer and unmet need was most distinctly defined. However, the mechanistic rationale for male use — MC4R-mediated central desire and arousal initiation, additive to peripheral PDE5 inhibitor effects — remains scientifically sound and is the basis for ongoing off-label clinical interest.
Safety Profile and Prescribing Considerations
The safety profile of bremelanotide is well-characterized from over 1,200 subjects in controlled trials plus open-label extension data.
Most common adverse events: Nausea (approximately 40% with first dose, decreasing with continued use), flushing (20-25%), headache (12%), injection site reactions (mild, 94% rated mild). Most adverse events were mild to moderate and transient.
Blood pressure effects: Bremelanotide produces transient blood pressure changes of approximately 3 to 6 mmHg mean decrease beginning approximately 30 minutes after injection and resolving within 12 hours. The contraindication to use in high-risk cardiovascular disease patients (uncontrolled hypertension, history of cardiovascular or cerebrovascular events) reflects this hemodynamic effect. The transient BP change was not clinically significant in the trial population but necessitates caution in subjects with compromised cardiovascular reserve.
Hyperpigmentation: Mild, transient facial flushing and hyperpigmentation occur in some subjects due to residual MC1R activity. These effects are substantially reduced compared to MT-2 and resolved following discontinuation.
Nausea management: Nausea is dose-related and most prominent with first-dose administration. Clinical experience suggests that nausea frequency and intensity decrease with continued as-needed use as subjects accommodate to the compound — consistent with the long-term safety data showing continued good tolerability through the 52-week extension.
Current Research Status
Bremelanotide (PT-141, Vyleesi) is FDA-approved for HSDD in premenopausal women and remains an active area of clinical research, including ongoing investigation of efficacy in male sexual dysfunction (off-label), complementary use with PDE5 inhibitors, and central melanocortin pharmacology. Post-marketing surveillance continues under FDA oversight. The compound also remains an important research tool for investigation of melanocortin CNS pharmacology, dopaminergic desire circuits, and the neurobiology of sexual motivation.
Reconstitution Note
PT-141 (bremelanotide) for research use is supplied as lyophilized powder. Bacteriostatic water is the standard reconstitution solvent. The pharmaceutical Vyleesi formulation is supplied as a pre-filled autoinjector at 1.75 mg/0.3 mL for subcutaneous administration — a concentration and formulation distinct from research-grade reconstituted powder. Always confirm the recommended solvent and concentration against the specific lot datasheet before reconstitution.
In-Use Period and Storage
Before Reconstitution — Lyophilized Powder
Rogue Compounds stores all products refrigerated prior to shipping to maintain compound integrity from production through to delivery. Upon receipt researchers should store vials at 2 to 8 degrees Celsius immediately. Keep vials sealed, dry, and away from direct light until ready for use. Do not freeze. Repeated freeze-thaw cycling has been documented in peer-reviewed pharmaceutical formulation literature to accelerate structural degradation even in dry powder form, potentially compromising molecular integrity and experimental reproducibility.
Why We Refrigerate Instead of Freeze
Freezing and thawing introduces mechanical and osmotic stress at the molecular level. Published pharmaceutical research identifies freeze-thaw cycling as a significant risk factor for loss of structural integrity in peptides and protein-based compounds. To protect compound quality at every stage of handling and fulfillment, Rogue Compounds maintains refrigerated rather than frozen cold chain storage throughout the entire process.
After Reconstitution — Liquid Solution
Store reconstituted solutions refrigerated at 2 to 8 degrees Celsius immediately after preparation. Protect from light. Avoid repeated freeze-thaw cycles. Use within the timeframe recommended for the individual compound. Label each aliquot with the compound name, concentration, date of reconstitution, and diluent used. Discard any solution that shows visible particulate matter, discoloration, or signs of degradation.
Note: Storage and in-use recommendations on this page are provided as general laboratory guidance based on standard peptide handling practices documented in peer-reviewed pharmaceutical literature. Researchers should always refer to the individual compound’s published research literature and datasheet for any specific requirements. All products sold by Rogue Compounds are intended strictly for in-vitro laboratory research use only.
Available from Rogue Compounds
View the PT-141 product page:
https://roguecompounds.com/product/pt-141/