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Bremelanotide: Recommended PT-141 Dosage for Results

pt 141 dosage

Sexual dysfunction can be devastating to both your own mental health and the relationship you have with your partner.

In the United States alone, 43% of women and 31% of men experience sexual problems.

Menopausal women usually experience hypoactive sexual desire disorder (HSDD), which negatively impacts their desire and fantasies for sexual intimacy. 

As for men, over 30 million Americans are affected by some form of erectile dysfunction (ED).

In addition to ruining their sex life, ED can also be an early warning sign of existing and/or future heart problems. 

The common solution is to turn to medications like Flibanserin, Viagra, and Cialis for stimulated sexual desire and improving performance in the bedroom.

A safer option for solving erectile dysfunction and hypoactive sexual desire disorder in men and women might be the peptide known as PT-141 (a.k.a. Bremelanotide).

PT-141 offers an alternative approach to treating sexual health problems by addressing one’s neurochemistry instead of penile blood flow. 

For some people, this shift can be a game-changer for improving sexual health and one’s overall quality of life.

In this article, we’ll dive deeper into the most optimal PT-141 dosage for enhancing libido and treating sexual dysfunction.

Additionally, we’ll discuss some health benefits of bremelanotide that expand beyond the domain of sexual health. 

What is PT-141 (Bremelanotide)?

pt 141 dosage

Bremelanotide, also known as PT-141, is an FDA-approved drug developed from the hormone Melanotan 2

This synthetic peptide activates internal pathways in the brain that play an important role in achieving a normal sexual response. 

It was originally used in tanning salons to help with skin pigmentation, but was later discovered to be able to treat sexual disorders such as hypoactive sexual desire disorder (HSDD, i.e. the persistent absence of sexual desire/fantasizing) and erectile dysfunction.

How PT-141 Works

pt 141 dosage

PT-141 works by activating melanocortin receptors, specifically MC4R (melanocortin-4 receptor), in the brain. 

MC4R helps regulate numerous functions such as sexual desire and arousal, mood, appetite, and thinking.

When PT-141 binds to MC4R, it triggers the release of neurochemicals such as dopamine that are involved in sexual desire. 

This biochemical cascade then sends signals to the hypothalamus that further boosts sexual arousal, desire, and satisfaction. 

In fact, in a study in the Journal of Clinical Investigation, 31 premenopausal heterosexual women with HSDD who were given MC4R experienced greater sexual desire for up to 24 hours.

There was also a reduction in self-consciousness alongside the enhancement of sexual imagery, making women with HSDD more responsive to erotic stimuli:

“During functional neuroimaging, MC4R agonism enhanced cerebellar and supplementary motor area activity and deactivated the secondary somatosensory cortex, specifically in response to visual erotic stimuli, compared with placebo. 

In addition, MC4R agonism enhanced functional connectivity between the amygdala and the insula during visual erotic stimuli compared with placebo.”

So for those of you with sexual issues that are affecting your relationship and performance in bed, PT-141 is worth a shot!

Are PT-141 Injections Safe?

pt 141 dosage

PT-141 is administered via subcutaneous injection in fat deposits, which are usually the thighs and stomach.

Doing so ensures that the drug is absorbed efficiently into the bloodstream so it can exert its biological effects quickly and effectively. 

As with any peptide injection, you can prevent skin problems and irritations by frequently rotating your injection sites.

Other good injection practices include NOT re-using the same needle to avoid contamination, and discarding an injection solution if it is cloudy/discolored.

Recommended PT-141 Dosage

pt 141 dosage

Before using PT-141, it’s crucial to follow the recommended dosage guidelines to ensure both safety and effectiveness.

According to the official product monograph:

“1.75 milligrams (mg) injected under the skin at least 45 minutes before a sexual activity.

Do not use more than one dose of this medicine within 24 hours. Do not use more than 8 doses per month (i.e. 2 injections within a week).”

However, in practice this starting dose will prove to be too high for many people.

If you’re brand new to PT-141, begin with a low dose of 0.5 mg.

This initial dose will allow your body to gradually adjust to the peptide’s effects, plus you can carefully monitor how your body reacts to PT-141. 

If you experience no adverse effects, you can slowly increase the dosage by increments of 0.5 mg to eventually land somewhere between 1 and 2 mg for ongoing maintenance.

However, do not exceed 2 mg per administration to avoid the risk of overdose.

PT 141 Dosage FAQ

pt 141 dosage

Have questions about dosing PT-141? We’ve answered them below.

When Should I Take PT-141?

If you want to enhance your performance in bed, it is recommended to take PT-141 (bremelanotide) approximately 45 minutes before engaging in sexual activity.

This timing allows the peptide to take effect at the right moment, helping you experience the benefits when you desire them the most. 

You also give the peptide enough time to stimulate the melanocortin receptors in the brain, which helps increase sexual desire and arousal. 

The end result is heightened physical and mental readiness for intimacy, leading to a much more satisfying sexual experience for yourself and your partner.

How Often Can You Take PT-141?

The effects of PT-141 can last up to 72 hours for every 2 mg dose. 

Due to its long duration of action, it’s recommended that you take only one dose of PT-141 per 24-hour period.

Remember: you can only use the peptide a maximum of three times a week and no more than eight times a month to minimize the risk of potential side effects.

What are the Adverse Effects of PT-141?

Bremelanotide side effects are very uncommon. However, some first-time users have reported the following side effects:

  • Headache
  • Joint stiffness
  • Facial flushing
  • Blurred vision
  • Vomiting
  • Temporary increase in blood pressure (systolic or diastolic blood pressure)

Since PT-141 can darken skin pigmentation, you may also develop a dark complexion around the gums and face (although this is exceedingly rare).

In any case, if you want a near guarantee for avoiding unwanted side effects, consult with your doctor first before adding PT-141 to your regimen. 

Be transparent about any of your pre-existing conditions or medications to avoid negative interactions. 

Is It Safe to Use PT-141 and Viagra Together?

Yes, PT-141 is safe to use with Viagra (sildenafil). 

While Viagra works by increasing blood flow to the penis, PT-141 operates through the central nervous system to increase sexual desire and arousal. 

The complementary mechanisms of these two medications can provide a more holistic approach to treating erectile dysfunction.

However, as with any medication, there is always the potential for interactions or adverse effects. 

So before using both compounds together, discuss your personal medical history with your doctor and disclose any additional medications you’re taking.

Your doctor can guide you on proper dosing and administration, which will reduce the likelihood of any potential side effects you may face while maximizing the benefits of PT-141.

Does PT-141 Treat Erectile Dysfunction?

Yes, bremelanotide (PT-141) can be used to treat erectile dysfunction and other sexual disorders in men. 

Unlike other ED treatments for men designed to improve blood flow to the penile tissue (ex. Cialis and Viagra),  bremelanotide acts on the central nervous system via targeting the melanocortin receptors in the brain. 

This helps increase sexual desire and arousal in men, but also addresses hypoactive sexual desire disorder in women who are afflicted with this condition.

Potential Benefits of PT-141 Peptide

pt 141 dosage

Boosts Sexual Health

In June 2019, the FDA approved bremelanotide for women with low sexual desire

This decision was made after many successful phase 3 trials that demonstrated its ability to increase sexual desire while reducing sexual distress in women diagnosed with HSDD 

This approval made bremelanotide the second drug to receive FDA approval for treating low sexual desire in premenopausal women (after Flibanserin). 

Since then, additional studies have reported the positive effects of PT-141 in women with sexual problems. 

In a study published in the Journal of Women’s Health, premenopausal women with low sexual desire and other dysfunctions who were given bremelanotide experienced improvement in their sexual desire after 12 weeks compared to the placebo group:

“Patients randomized to receive placebo or BMT 0.75, 1.25 or 1.75 mg self-administered subcutaneously, as desired, over 12 weeks. 

Primary end point was change in satisfying sexual events/month. Secondary end points included total score changes on female sexual function index and female sexual distress scale-desire/arousal/orgasm. 

Efficacy data, n = 327. For 1.25/1.75-mg pooled versus placebo, mean changes from baseline to study end were +0.7 versus +0.2 satisfying sexual events/month (p = 0.0180), +3.6 versus +1.9 female sexual function index total score (p = 0.0017), −11.1 versus −6.8 female sexual distress scale-desire/arousal/orgasm total score (p = 0.0014). 

Adverse events: nausea, flushing, headache. Conclusion: In premenopausal women with female sexual dysfunctions, self-administered, as desired, subcutaneous BMT was safe, effective, and well tolerated.”

And similar to ED medications, bremelanotide can also help men who struggle to get and maintain an erection.

In fact, it can trigger an erection without reliance on visual or tactile sexual stimulation: 

“Bremelanotide (PT-141) is a metabolite of MT2 which was developed later in response to the discovery that MT2 was able to induce erections in men. 

Bremelanotide appears to act on melanocortin receptor- 3 (MCR-3) and MCR-4 receptors in the CNS, where it enhances sexual arousal and penile erections through the release of dopamine. 

The central actions of this drug also make it suitable for the treatment of certain female sexual dysfunction.

The CNS site of action of these compounds was demonstrated in preclinical experimental models in which MT2 did not relax rabbit corpus cavernosum strips, and direct intracavernosal injection of MT2 failed to alter ICP in rats.

It has been shown in a double-blind, placebo-controlled study that the subcutaneous administration of MT2 to men with organic and psychogenic ED-induced penile erections in the absence of visual or tactile sexual stimulation. 

From a clinical perspective, the potential utility of MT2 is limited by its route of administration (subcutaneous) and onset of action (>90 min).

Bremelanotide is available as an atomizer for intranasal administration, and response to the peptide is rather immediate, initiating a penile response in a matter of minutes. 

Both phase I and phase II trials have been completed for bremelanotide. 

In a 12-week phase IIb trial recruiting 726 non-diabetic men with ED, IIEF EF domain scores were significantly higher in subjects who received bremelanotide 5 mg relative to those who received a placebo.

Bremelanotide also has efficacy in producing erections in men with diabetes and those who do not respond to sildenafil.

When used for therapy in ED, both MT2 and bremelanotide are unlikely to enhance skin pigmentation or cause satiety under normal use as these effects typically require prolonged dosing.”

Promotes Fat Loss

Outside of improving sexual health, PT-141 may promote weight loss.

Overweight premenopausal women who were given PT-141 twice a day saw reduced mean body weight after 16 days of treatment compared to the placebo group, as shown in the Journal of Diabetes, Obesity and Metabolism:

“The melanocortin 4 receptor (MC4R) plays a central role in appetite regulation, and agonistic activity at this receptor promotes satiety. 

Results from two randomized controlled clinical trials examine the effects of bremelanotide’s agonism at MC4R on caloric intake and body weight.

Premenopausal women with a body mass index >30 kg/m2 were studied in two phase 1, single‐centre, randomized, double‐blind, placebo‐controlled trials. 

Study A matched subjects 1:1 to receive subcutaneous placebo or bremelanotide three times daily for days 1‐15. 

Study B was a crossover trial with six distinct treatment sequences consisting of three 4‐day treatment periods, investigating once‐a‐day and twice‐a‐day exposure to bremelanotide versus placebo. 

Subjects received one of the three treatments twice‐daily during each period: 0 mg/0 mg, 2.5 mg/0 mg or 2.5 mg/2.0 mg bremelanotide. 

Body weight and food intake were recorded in detail daily. Adverse events were recorded throughout both studies.

In Study A, 27 of 30 bremelanotide subjects (90.0%) completed the trial and exhibited a significantly greater reduction in body weight after 16 days versus placebo [least squares mean difference (95% CI), −1.3 (−1.9 to −0.8) kg; p < .0001]. 

Mean caloric intake in bremelanotide subjects was decreased versus placebo, with a magnitude of reduction of approximately 400 kcal/day throughout Study A (p < .01). 

In Study B, 15 of 27 subjects (55.6%) completed all three phases. 

Significantly greater reduction of mean body weight occurred in twice‐daily bremelanotide subjects versus placebo (1.7 vs. 0.9 kg, respectively, p < .001). 

Total caloric intake reduction was significantly greater in the bremelanotide groups versus placebo (mean difference range: 398‐469 kcal; p < .0001).”

Similarly, in a study in the Journal of Diabetes, obese Rhesus macaque monkeys given a melanocortin receptor agonist decreased their food intake by 35% and lost weight over 8 weeks of treatment. 

The test animals not only decreased their body’s adiposity, but they also maintained adequate glucose tolerance.

Researchers reported no side effects on the heart rate or blood pressure:

“Importantly, we observed no increases in blood pressure or heart rate 

Activation of MC4R causes dramatic weight loss in rodent models, and mutations in humans are associated with obesity. 

This makes MC4R a logical target for pharmacological therapy for the treatment of obesity. 

However, previous studies in rodents and humans have observed a broad array of side effects caused by acute treatment with MC4R agonists, including increased heart rate and blood pressure. 

We demonstrate that treatment with a highly-selective novel MC4R agonist (BIM-22493 or RM-493) resulted in transient decreases in food intake (35%), with persistent weight loss over 8 weeks of treatment (13.5%) in a diet-induced obese nonhuman primate model. 

Consistent with weight loss, these animals significantly decreased adiposity and improved glucose tolerance. 

Importantly, we observed no increases in blood pressure or heart rate with BIM-22493 treatment. 

In contrast, treatment with LY2112688, an MC4R agonist previously shown to increase blood pressure and heart rate in humans, caused increases in blood pressure and heart rate, while modestly decreasing food intake.”

Supports Brain and Cognitive Health

Some early research indicates PT-141 could help improve cognitive health. 

A study in the Annals of New York Academy of Sciences showed that melanocortin receptor agonists interact with brain chemicals such as dopamine, oxytocin, serotonin, and corticotropin-releasing factors.

This could lead to improvements in socioemotional behaviors and cognitive skills: 

“It is now established that the hypothalamus is essential in coordinating endocrine, autonomic, and behavioral responses to changes in energy availability. 

However, the interaction of key peptides, neuropeptides, and neurotransmitters systems within the hypothalamus has yet to be delineated. 

Recently, we investigated the mechanisms through which central serotonergic (5-hydroxytryptamine, 5-HT) systems recruit leptin-responsive hypothalamic pathways, such as the melanocortin systems, to affect energy balance. 

Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we found that 5-HT drugs require functional melanocortin pathways to exert their effects on food intake. 

Specifically, we observed that anorectic 5-HT drugs activate pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (Arc). 

We provide evidence that the serotonin 2C receptor (5-HT2CR) is expressed on POMC neurons and contributes to this effect. Finally, we found that 5-HT drug-induced hypophagia is attenuated by pharmacological or genetic blockade of downstream melanocortin 3 and 4 receptors. 

We review candidate brain regions expressing melanocortin 3 and 4 receptors that play a role in energy balance. 

A model is presented in which activation of the melanocortin system is downstream of 5-HT and is necessary to produce the complete anorectic effect of 5-HT drugs. 

The data reviewed in this paper incorporate the central 5-HT system to the growing list of metabolic signals that converge on melanocortin neurons in the hypothalamus.”

Similarly, melanocortin receptor agonists also boosted social information processing and social reinforcement in mice models, as evidenced in a study in The Journal of Neuroscience.

“The peptides α-melanocyte stimulating hormone (α-MSH) and oxytocin, when administered centrally, produce similar behavioral effects. α-MSH induces Fos expression in supraoptic oxytocin neurons, and α-MSH melanocortin-4 receptors (MC4Rs) are highly expressed in the supraoptic nucleus, suggesting that α-MSH and oxytocin actions are not independent. 

Here we investigated the effects of α-MSH on the activity of supraoptic neurons. 

We confirmed that α-MSH induces Fos expression in the supraoptic nucleus when injected centrally and demonstrated that α-MSH also stimulates Fos expression in the nucleus when applied locally by retrodialysis. 

Thus α-MSH-induced Fos expression is not associated with electrophysiological excitation of supraoptic neurons because central injection of α-MSH or selective MC4 receptor agonists inhibited the electrical activity of oxytocin neurons in the supraoptic nucleus recorded in vivo. 

Consistent with these observations, oxytocin secretion into the bloodstream decreased after central injection of α-MSH. 

However, MC4R ligands induced substantial release of oxytocin from dendrites in isolated supraoptic nuclei. 

Because dendritic oxytocin release can be triggered by changes in [Ca2+] I, we measured [Ca2+] I responses in isolated supraoptic neurons and found that MC4R ligands induce a transient [Ca2+] I increase in oxytocin neurons. 

This response was still observed in low extracellular Ca2+ concentration and probably reflects mobilization of [Ca2+] I from intracellular stores rather than entry via voltage-gated channels. 

Taken together, these results show for the first time that a peptide, here α-MSH, can induce differential regulation of dendritic release and systemic secretion of oxytocin, accompanied by dissociation of Fos expression and electrical activity.”

Maintaining Healthy Blood Sugar Levels

Melanocortin receptor agonists such as PT-141 can help protect against the onset of diabetes and the negative effects of high blood sugar.

This is because melanocortin receptor agonists boost the body’s response to insulin (insulin sensitivity), thereby counteracting high blood sugar levels:

“Melanocortin receptor agonists act in the brain to regulate food intake and body weight and, independently of these actions, affect insulin sensitivity. 

These experiments investigated the function of novel non-selective melanocortin receptor agonists (BIM-22493, BIM-22511) that cross the blood-brain barrier when administered peripherally. 

Treatment of diet-induced obese C57BL/6J (B6) mice with melanocortin agonists administered peripherally improved obesity, hyperinsulinemia (∼50%), and fatty liver disease. 

The specificity of function was determined using B6 melanocortin-3 and melanocortin-4 receptor knockout mice (MC3RKO, MC4RKO). Chow-fed MC4RKO but not MC3RKO used for these tests exhibited obesity, hyperinsulinemia, and severe hepatosteatosis associated with increased expression of insulin-stimulated genes involved in lipogenesis. 

Reduced food intake associated with acute BIM-22493 treatment, and weight loss associated with 14d of treatment with BIM-22511, required functional MC4R but not MC3R. 

However, while 14d of treatment BIM-22511 did not affect body weight and even increased cumulative food intake in MC4RKO, a significant reduction (∼50%) in fasting insulin was still observed. 

Despite lowering insulin, chronic treatment with BIM-22511 did not improve hepatosteatosis in MC4RKO and did not affect hepatic lipogenic gene expression. 

Together, these results demonstrate that peripherally administered melanocortin receptor agonists regulate body weight, liver metabolism, and glucose homeostasis through independent pathways. 

MC4R are necessary for melanocortin agonist-induced weight loss and improvements in liver metabolism but are not required for improvements in hyperinsulinemia. 

Agonists with activity at MC4R improve glucose homeostasis at least partially by causing weight loss, however, other melanocortin receptors may have potential for treating aberrations in glucose homeostasis associated with obesity.”

In another study published in the Journal of Life Sciences, murine models with obesity and type 2 diabetes saw improved blood sugar tolerance and reduced insulin levels after treatment with melanocortin receptor agonists:

“We examined the effect of intracerebroventricular (i.c.v.) injection of MTII, a melanocortin agonist, on hepatic gene expression in a mouse model of insulin-deficient diabetes. 

Diabetes was induced in male C57BL/6J mice by intraperitoneal injections of streptozotocin (STZ). 

Diabetic mice received daily i.c.v. injections of MTII (3 nmol) for 11 days. Hepatic expression levels of lipogenic genes and their transcription factors were measured.

MTII treatment significantly reduced hepatic expression levels of genes encoding lipid biosynthetic enzymes, stearoyl-CoA desaturase 1 (SCD1), glycerol-3-phosphate acyltransferase 1 (GPAT1), acyl-CoA: diacylglycerol acyltransferase 1 (DGAT1), and DGAT2 mRNA without significant changes in serum insulin levels, homeostasis model assessment of insulin resistance (HOMA-IR) and glucose tolerance in STZ-induced diabetic mice. 

MTII treatment also reduced fatty acid synthase (FAS) and SCD1 protein levels in the liver of diabetic mice. 

Expression levels of genes encoding transcription factors of these lipogenic genes, sterol regulatory element-binding protein 1c (SREBP-1c), and peroxisome proliferator-activated receptor γ2 (PPARγ2) were also significantly reduced by MTII treatment.

These data suggest that the insulin-independent mechanism is involved in the regulation of hepatic lipogenic gene expression. 

Enhanced central melanocortin signaling may be effective in improving abnormal lipid metabolism associated with insulin deficiency or insulin-insufficiency.”

Supports Eye Health

High blood sugar can also affect specialized neurons in the retina known as photoreceptor cells.

Fortunately, melanocortin receptor agonists can help protect eye health from possible damage caused by increased blood sugar levels. 

In a study published in the Journal of Cellular and Molecular Medicine, melanocortin receptor agonists guarded the eyes of mice from the harmful effects of high blood sugar levels.

Within this context, these agonists work by reducing inflammatory cytokines and chemokines, thereby, supporting photoreceptor integrity:

“Retinal photoreceptors are particularly vulnerable to local high‐glucose concentrations. Oxidative stress is a risk factor for diabetic retinopathy development. 

Melanocortin receptors represent a family of G‐protein‐coupled receptors classified into five subtypes and are expressed in the retina. 

Our previous data indicate that subtypes 1 and 5 receptor agonists exert a protective role on experimental diabetic retinopathy. 

This study focuses on their role in primary retinal cell cultures in high‐glucose concentrations. 

After eye enucleation from wild‐type male C57BL/6 mice, retinal cells were isolated, plated in high‐glucose concentration, and treated with melanocortin receptors 1 and 5 agonists and antagonists. 

Immunocytochemical and biochemical analysis showed that treatment with melanocortin receptors 1 and 5 agonists reduced anti‐inflammatory cytokines and chemokines and enhanced manganese superoxide dismutase and glutathione peroxidase levels, preserving photoreceptor integrity. 

According to this evidence, we propose a major role of melanocortin receptors 1 and 5 on primary retinal cell response against high glucose or oxidative insults.”

The melanocortin receptor agonists also help protect the retinal vascular network by stopping local inflammatory and immune responses, which are also induced by high blood sugar levels:

“We hypothesize that melanocortin receptors (MC) could activate tissue protective circuits in a model of streptozotocin- (STZ-) induced diabetic retinopathy (DR) in mice. 

At 12–16 weeks after diabetes induction, fluorescein angiography (FAG) revealed an approximate incidence of 80% microvascular changes, typical of DR, in the animals, without signs of vascular leakage. 

Occludin progressively decreased in the retina of mice developing retinopathy. qPCR of the murine retina revealed the expression of two MC receptors, Mc1r and Mc5r. 

The intravitreal injection (5 μL) of the selective MC1 small molecule agonist BMS-470539 (33 μmol) and the MC5 peptidomimetic agonist PG-901 (7.32 nM) elicited significant protection with regular course and caliber of retinal vessels, as quantified at weeks 12 and 16 after diabetes induction. 

Mouse retina homogenate settings indicated an augmented release of IL-1α, IL-1β, IL-6, MIP-1α, MIP-2α, MIP-3α, and VEGF from diabetic compared to nondiabetic mice. 

Application of PG20N or AGRP and MC5 and MC1 antagonists, respectively, augmented the release of cytokines, while the agonists BMS-470539 and PG-901 almost restored the normal pattern of these mediators back to nondiabetic values. 

Similar changes were quantified with respect to Ki-67 staining. Finally, the application of MC3-MC4 agonists/antagonists resulted in being inactive with respect to all parameters under assessment.”

Helps with Alcohol Addiction

Believe it or not, some researchers are looking into PT-141 for the treatment of alcohol addiction through modulating voluntary ethanol (alcohol) consumption. 

Melanocortin receptor agonists such as bremelanotide work with the melanocortin 4 receptor (MC4R) to reduce voluntary ethanol in binge-like drinking, as evidence in a study involving mice: 

“Recent data have implicated the melanocortin (MC) system in modulating voluntary ethanol consumption. 

Administration of melanotan-II (MTII), a nonselective melanocortin receptor (MCR) agonist, reduces voluntary ethanol consumption in C57BL/6J mice. 

Previous studies have demonstrated that central infusion of MTII effectively reduced voluntary ethanol drinking in mutant mice lacking normal expression of MC3R (MC3R−/− mice) but failed to alter ethanol drinking in mice lacking expression of MC4R, demonstrating that central MTII administration reduces voluntary ethanol drinking by signaling through the MC4R. 

However, evidence shows that the neurocircuitry recruited during excessive binge-like ethanol drinking versus moderate ethanol drinking are not identical. 

Thus the present study sought to investigate the potential role of the MC3R in binge-like ethanol intake. 

To this end, the “drinking in the dark” (DID) procedure, a commonly used animal model of binge-like ethanol drinking, was employed. Wild-type MC3R+/+ and MC3R−/− mice were given intracerebroventricular (i.c.v.) infusion of MTII (0.0, 0.25, 0.50, or 1.0 μg) prior to the onset of a four-hour testing period in which mice were given access to 20% (v/v) ethanol. 

Immediately after the four-hour testing period, tail blood samples were collected from each animal in order to assess blood ethanol concentrations (BECs). 

Consistent with previous findings, central administration of MTII blunted binge-like ethanol drinking in both MC3R+/+ and MC3R−/− mice. Interestingly, all doses of MTII blunted binge-like ethanol drinking in MC3R−/− mice during the first hour of testing, while only the 1.0 μg dose reduced binge-like drinking in MC3R+/+ mice. 

Thus, MC3R−/− mice were more sensitive to the protective effects of MTII. 

These data suggest that MC3Rs oppose the protective effects of MTII against binge-like ethanol drinking, and thus selective MC3R antagonists may have potential therapeutic roles in treating excessive ethanol drinking.”

Boosts Immune System Function

Lastly, bremelanotide can also strengthen the immune system by boosting the activities of immune system cells, such as monocytes, neutrophils, B-lymphocytes, dendritic cells, and white blood cells:

“To investigate the relevance of adrenocorticotrophic hormone (ACTH) therapy in human gouty arthritis, we have tested the effect of several ACTH-related peptides in a murine model of experimental gout. 

Systemic treatment of mice with ACTH4-10 (MEHFRWG) (10-200 microgram s. c.) inhibited neutrophil accumulation without altering peripheral blood cell counts or circulating corticosterone levels. 

A similar effect was seen with alpha- and beta-melanocyte-stimulating hormones (1-30 microgram s.c.). 

In vivo, the release of the chemokine KC-(detected in the lavage fluids before the maximal influx of neutrophils) was significantly reduced (-50 to -60%) by ACTH4-10. 

Macrophage activation in vitro, determined as phagocytosis and KC release, was inhibited by ACTH and ACTH4-10 with approximate IC50 values of 30 nM and 100 microM, respectively. 

The melanocortin receptor type 3/4 antagonist SHU9119 prevented the inhibitory actions of ACTH4-10 both in vitro and in vivo. 

However, melanocortin type 3, but not type 4, receptor mRNA was detected in mouse peritoneal macrophages by RT-PCR. 

Therefore, we propose that activation of this receptor type by ACTH4-10 and related amino acid sequences attenuates KC release (and possibly the production of other cytokines) from macrophages with consequent inhibition of the host inflammatory response, thus providing a notional anti-inflammatory mechanism for ACTH that is unrelated to stimulation of glucocorticoid release.”

Jay’s Closing Thoughts

As I elucidated in my original article about the PT-141 peptide, its benefits for sexual health regardless of gender are well-documented.

It is truly one of the few peptides that serve a singular purpose and do so effectively.

While I AM personally a non-responder to PT-141, there are clearly many individuals who have noticed a dramatic improvement in both sexual desire and performance.

But getting to the “sweet spot” (no pun intended) will require experimenting with the dose according to the instructions I laid out earlier in this article.

Some people will get all they desire from the lowest dose possible, while others will have to ramp their injections up to the highest permissible dose.

As for the other health benefits outside of libido and erectile dysfunction… don’t get too excited just yet.

There is a LOT of validation that will have to be done in the real world and the laboratory for said benefits to have any weight to them.

Yet it’s entirely possible this could change… just like how the GLP-1 peptides were merely medications for diabetes before becoming effective tools for weight loss, behavioral addictions, and much more.

So don’t give up hope on PT-141 becoming a “Swiss army knife” peptide just yet!

Closing Thoughts on Bremelanotide

pt 141 dosage

PT-141 or bremelanotide, when used correctly, can boost your sexual desire and arousal to lead to improvements in your sexual health and/or performance. 

But no matter what, make sure you use the correct dosage of PT-141 to maximize its benefits while minimizing the likelihood of any side effects.

And always consult with your doctor to tailor the dosage to your specific needs if you are uncomfortable doing so by yourself.

Lastly, while you should be buying PT-141 from Limitless Life Nootropics, you can only do so as a member of the free-to-join JayC VIP Insider Club:

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