97559-35-8 Usage
General Description
NEUROKININ A (4-10) is a neuropeptide derived from the larger precursor protein, neurokinin A. It acts as a neurotransmitter in the nervous system, particularly in the transmission of pain signals. The peptide is involved in various physiological processes, including the regulation of blood pressure, smooth muscle contraction, and the secretion of hormones. NEUROKININ A (4-10) also plays a role in the immune response and inflammation. It exerts its effects through binding to neurokinin receptors, particularly the neurokinin 2 receptor, and is implicated in the pathophysiology of a range of conditions, including chronic pain and neurogenic inflammation. Research into the potential therapeutic applications of NEUROKININ A (4-10) is ongoing, particularly in the development of new treatments for pain and inflammation.
Check Digit Verification of cas no
The CAS Registry Mumber 97559-35-8 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 9,7,5,5 and 9 respectively; the second part has 2 digits, 3 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 97559-35:
(7*9)+(6*7)+(5*5)+(4*5)+(3*9)+(2*3)+(1*5)=188
188 % 10 = 8
So 97559-35-8 is a valid CAS Registry Number.
InChI:InChI=1/C34H54N8O10S/c1-18(2)13-23(31(49)39-22(29(36)47)11-12-53-5)38-26(44)16-37-34(52)28(19(3)4)42-32(50)24(14-20-9-7-6-8-10-20)40-33(51)25(17-43)41-30(48)21(35)15-27(45)46/h6-10,18-19,21-25,28,43H,11-17,35H2,1-5H3,(H2,36,47)(H,37,52)(H,38,44)(H,39,49)(H,40,51)(H,41,48)(H,42,50)(H,45,46)/t21-,22-,23-,24-,25-,28-/m0/s1
97559-35-8Relevant articles and documents
A New Class of High Affinity Ligands for the Neurokinin A NK2 Receptor: ψ(CH2NR) Reduced Peptide Bond Analogues of Neurokinin A4-10
Harbeson, Scott L.,Shatzer, Scott A.,Le, Tieu-Binh,Buck, Stephen H.
, p. 3949 - 3955 (1992)
Analogues of 10>NKA4-10 were synthesized in which each of the amide bonds was sequentially replaced with the reduced amide ψ(CH2NH) bond to determine the effect of this structural modification on the antagonism of NKA binding to
