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| Trade names | Semax |
| Other names | L-Methionyl-L-α-glutamylhistidyl-L-phenylalanyl-L-prolylglycyl-L-proline, (Pro8,Gly9,Pro10)ACTH-(4-10), H-Met-Glu-His-Phe-Pro-Gly-Pro-OH, MEHFPGP, H-MEHFPGP-OH |
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| Formula | C37H51N9O10S |
| Molar mass | 813.93 g·mol−1 |
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Semax is amedication which is used inEastern Europe for the treatment of a broad range ofconditions likebrain trauma but predominantly for its claimednootropic,neuroprotective, and neurorestorative effects.[1]
Themechanism of action of Semax is unknown.[2][3] It might interact with certainmelanocortin receptors orinhibit enkephalinaseenzymes.[2][3] Chemically, Semax is apeptide and asyntheticanalogue of a fragment ofadrenocorticotropic hormone (ACTH).[4][5]
Semax was first described by 1991.[5] Although used as aprescription drug inRussia, Semax has not been evaluated, approved for use, or marketed in most other countries.[6][7] The drug is widely sold byonline vendors and used as a purportednootropic (cognitive enhancer).[1][8]
Semax[9] has undergone extensive study in Russia and is on the RussianList of Vital & Essential Drugs approved by the Russian Federation government on 7 December 2011.[10] Medical uses for Semax include treatment ofstroke,transient ischemic attack,memory andcognitive disorders,peptic ulcers,optic nerve disease, and to boost theimmune system.[11][12][13][14]
In animals, Semax rapidly elevates the levels andexpression ofbrain-derived neurotrophic factor (BDNF) and its signaling receptortropomyosin receptor kinase B (TrkB) in thehippocampus,[15] and rapidly activatesserotonergic anddopaminergic brain systems.[16][17] Accordingly, it has been found to produceantidepressant-like andanxiolytic-like effects,[18][19] attenuate the behavioral effects of exposure tochronic stress,[18][19] andpotentiate the locomotor activity produced byD-amphetamine.[17][20] As such, it has been suggested that Semax may be effective in the treatment ofdepression.[21]
Though the exactmechanism of action of Semax is unclear, there is evidence that it may act throughmelanocortin receptors. Specifically, there is a report of Semaxcompetitively antagonizing the action ofα-melanocyte-stimulating hormone (α-MSH) at theMC4 andMC5 receptors in bothin vitro andin vivo experimental conditions, indicating that it may act as anantagonist orpartial agonist of these receptors. (&alpha-MSH acts as a full agonist of all five melanocortin receptors).[2] Semax did not antagonize α-MSH at theMC3 receptor, though this receptor could still be a target of the drug.[2] As for theMC1 andMC2 receptors, they were not assayed.[2]
In addition to actions at receptors, Semax, as well as a related peptide drug,Selank, have been found to inhibitenzymes involved in the degradation ofenkephalins and otherendogenous regulatorypeptides (IC50 = 10 μM), though the clinical significance of this property is uncertain.[3]
As a peptide, Semax has poororalbioavailability and hence is administeredparenterally as anasal spray or subcutaneous injection.
Semax is aheptapeptide andsyntheticanalogue of a fragment ofadrenocorticotropic hormone (ACTH), ACTH (4-10), of the followingamino acid sequence: Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP in single-letter form).[4]
Semax was first described inscientific literature by 1991.[5]
Semax is composed of sevenamino acid residues: Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP), which is reflected in the name - from an abbreviation of "seven amino acids"—in Russian: СЕМь АминоКиСлот—СЕМАКС.
