MIF-1 (Pro-Leu-Gly-NH2) Dosage Calculator
MIF-1, also known as melanostatin or PLG (Pro-Leu-Gly-NH2), is a naturally occurring tripeptide first isolated from hypothalamic extracts in the 1970s.
5mcg · Daily
Summary: Add 2mL BAC water to your 10mg vial. Draw to 0.1 units on a U-100 syringe for a 5mcg dose. This vial will last 2000 doses.
Cycle Planner
MIF-1 (Pro-Leu-Gly-NH2) Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = ~2 hours (functional CNS duration); plasma stability ~5 daysDisclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
MIF-1 (Pro-Leu-Gly-NH2) Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 5mg | Daily |
| Moderate | 10mg | Daily |
| Aggressive | 10mg | 2x Daily |
Note: MIF-1 (melanostatin, PLG) is an endogenous tripeptide derived from oxytocin cleavage. It displays an inverted U-shaped dose-response curve — higher doses can paradoxically reduce effectiveness. Clinical trials used 10 mg subcutaneous injections daily for 5-10 days for depression. The peptide is unusually resistant to plasma degradation and crosses the blood-brain barrier readily, though oral bioavailability is poor.
About MIF-1 (Pro-Leu-Gly-NH2)
MIF-1, also known as melanostatin or PLG (Pro-Leu-Gly-NH2), is a naturally occurring tripeptide first isolated from hypothalamic extracts in the 1970s. It was originally identified as a factor that inhibits the release of melanocyte-stimulating hormone (MSH) from the pituitary, but subsequent research revealed a much broader pharmacological profile centered on dopaminergic and opioidergic modulation in the brain. MIF-1 is derived from the enzymatic cleavage of oxytocin and is present endogenously in the central nervous system. The peptide acts as a positive allosteric modulator of the dopamine D2 and D4 receptor subtypes, binding to a site distinct from the primary dopamine binding site. This mechanism differentiates it from direct dopamine agonists and gives it a unique therapeutic profile. At the same time, MIF-1 blocks opioid receptor activation, which contributes to its antidepressant and anti-analgesic properties. Clinical trials in the 1980s and 1990s demonstrated that MIF-1 could match the antidepressant efficacy of imipramine, with notably faster onset of action — often producing measurable improvement within the first week of treatment. A double-blind study found that 8 of 9 patients receiving 10 mg subcutaneous MIF-1 daily achieved marked improvement on the Hamilton Depression Scale, compared to just 2 of 11 on placebo. Research has also explored MIF-1's potential in Parkinson's disease, given its dopamine-modulating properties, as well as its ability to attenuate neuroleptic-induced extrapyramidal side effects such as tardive dyskinesia in preclinical models. Brain mapping studies show that peripheral MIF-1 administration activates regions tied to mood regulation, memory, and anxiety processing — including the cingulate cortex, hypothalamus, amygdala, and nucleus accumbens.