Γ-Melanocyte-stimulating hormone

γ-Melanocyte-stimulating hormone
Names
	IUPAC name L-Tyrosyl-L-valyl-L-methionylglycyl-L-histidyl-L-phenylalanyl-L-arginyl-L-tryptophyl-L-α-aspartyl-L-arginyl-L-phenylalaninamide
	Other names gamma-MSH, γ-melanotropin, γ-melanocortin, γ-intermedin
Identifiers
CAS Number	72629-65-3;
3D model (JSmol)	Interactive image;
ChemSpider	24603539;
PubChem CID	16146269;
CompTox Dashboard (EPA)	DTXSID30657546 ;
	InChI InChI=1S/C74H99N21O16S/c1-41(2)62(95-63(102)49(75)30-44-22-24-47(96)25-23-44)72(111)90-53(26-29-112-3)64(103)84-38-59(97)87-57(34-46-37-80-40-86-46)70(109)92-55(32-43-16-8-5-9-17-43)68(107)88-52(21-13-28-82-74(78)79)67(106)93-56(33-45-36-83-50-19-11-10-18-48(45)50)69(108)94-58(35-60(98)99)71(110)89-51(20-12-27-81-73(76)77)66(105)91-54(65(104)85-39-61(100)101)31-42-14-6-4-7-15-42/h4-11,14-19,22-25,36-37,40-41,49,51-58,62,83,96H,12-13,20-21,26-35,38-39,75H2,1-3H3,(H,80,86)(H,84,103)(H,85,104)(H,87,97)(H,88,107)(H,89,110)(H,90,111)(H,91,105)(H,92,109)(H,93,106)(H,94,108)(H,95,102)(H,98,99)(H,100,101)(H4,76,77,81)(H4,78,79,82)/t49-,51-,52+,53-,54-,55-,56-,57-,58-,62-/m0/s1 Key: GZWUQPQBOGLSIM-XEMHBVLISA-N;
	SMILES CC(C)[C@@H](C(=O)N[C@@H](CCSC)C(=O)NCC(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CC2=CC=CC=C2)C(=O)N[C@H](CCCNC(=N)N)C(=O)N[C@@H](CC3=CNC4=CC=CC=C43)C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CC5=CC=CC=C5)C(=O)NCC(=O)O)NC(=O)[C@H](CC6=CC=C(C=C6)O)N;
Properties
Chemical formula	C74H99N21O16S
Molar mass	1570.80 g·mol−1
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references

γ-Melanocyte-stimulating hormone (γ-MSH) is an endogenous peptide hormone and neuropeptide. It is a melanocortin, specifically, one of the three types of melanocyte-stimulating hormone (MSH), and is produced from proopiomelanocortin (POMC). It is an agonist of the MC₁, MC₃, MC₄, and MC₅ receptors. It exists in three forms, γ₁-MSH, γ₂-MSH, and γ₃-MSH.

γ-MSH regulated cardiovascular functions. γ-MSH effects are measured through the effects it has on the central neural pathway dispersed throughout the kidney. It is not moderated based on tubular sodium transport. Gamma-MSH activates MC3R in renal tubular cells by limiting sodium absorption by inhibiting the central neural pathway. This regulates sodium balance and blood pressure. If MC3R is absent then there is resistance in γ-MSH which results in hypertension on HSD.