MIF-1

MIF-1 (Peptide) – Product Details

MIF-1, or Melanocyte-Inhibiting Factor-1, is a neuropeptide associated with regulating various physiological pathways, including dopaminergic and serotonergic systems. Derived from the precursor protein pro-opiomelanocortin (POMC), MIF-1 plays a role in modulating neurotransmitter dynamics in clinical models. Ongoing research explores its potential implications in addressing central nervous sy, attracting interest in scientific and medical investigations.

• CAS Number: 478336-92-4
• Molar Mass: 284.35 g/mol
• Chemical Formula: C₁₅H₂₅F₃N₄O₅
• IUPAC Name: Pro-Leu-Gly-NH2

What is MIF-1?

Melanostatin, or MIF-1 (Melanocyte-inhibiting factor), is an intrinsic bioactive peptide formed through the cleavage of oxytocin. Unlike its precursor, MIF-1 has diverse properties, acting as both an opioid receptor antagonist and a positive allosteric modulator of G-protein coupled receptors (specifically D2 and D4). It may also inhibit the release of peptide hormones like alpha-MSH and modulate melatonin receptor activity in experimental models during the trials. This peptide demonstrates a multifaceted profile, offering cognitive facilitation and dopaminergic modulation in research models during investigation in the laboratory.

Researchers explore related peptides like Tyr-MIF-1 and endomorphin-1 and -2, providing a broader understanding of their interconnected roles. In addition, Melanostatin, known for modulating the pathways of melanocyte-stimulating hormone secretion, is identified as a specific tripeptide, L-prolyl-L-leucylglycinamide, in laboratory models and clinical studies. Sharing similarities with the end part of oxytocin, Melanostatin potentiates the effects of L-dopa and 5-hydroxytryptophan, mitigating induced tremors in subjects used in the laboratory trials.

How Does MIF-1 Work?

In the central nervous system (CNS), melanostatin (MIF-1), a naturally occurring tripeptide (Pro-Leu-Gly-NH2), is an important positive allosteric modulator (PAM) of dopamine D2 receptors (D2R). By attaching to allosteric regions, this modulation causes conformational changes that improve the affinity with which orthosteric ligands bind to the receptor. Although MIF-1 is known to have potential uses in dopaminergic pathway dysregulation models, it has drawbacks including low stability against enzymes produced by the central nervous system and low gastrointestinal absorption, which makes oral administration in experimental subjects difficult.

Studies investigated a bioisosteric replacement of cyclic β-amino acids with the prolyl residue as a means of improving MIF-1’s absorption, distribution, metabolism, and excretion (ADME) characteristics without compromising its PAM activity in order to solve these problems. This alteration resulted in the design, synthesis, and pharmacological assessment of six new MIF-1 proline mimetics. During functional tests at D2R, one of these peptidomimetics outperformed MIF-1 neuropeptide at 1 nM in terms of performance (lower EC50). Crucially, in human-derived neuroblastoma SH-SY5Y cell lines, this compound did not show any cytotoxic effects at 100 µM.

Studies are being conducted to evaluate this promising proline mimetic’s chemical stability and in vitro biological permeability. It now has more options to create alternative dopaminergic signaling modulators because of the identification of a strong D2R PAM with a good toxicological profile.

In the context of melanostatin’s effects, its ability to influence neuromodulatory activity and monoaminergic transmission pathways underscores its potential interactions with the blood–brain interface. Melanostatin’s capacity to modulate brain dopamine levels and its metabolite, homovanilic acid, suggests that it has the potential to interact with the brain’s neurochemical environment. This interaction could involve melanostatin crossing the blood–brain interface or affecting the interface’s permeability to certain molecules. Although the precise mechanism by which melanostatin influences the interface remains to be fully elucidated, its impact on monoamine concentrations indicates that it interacts with the brain at a molecular level.

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