Y-27632 dihydrochloride

• CAT Number: I010113
• CAS Number: 129830-38-2
• Molecular Formula: C14H21N3O • 2HCl
• Molecular Weight: 320.30
• Purity: ≥95%
• Synonyms: Y27632; Y-27632; Y 27632; Y27632 HCl; Y27632 dihydrochloride;(1R,4r)-4-((R)-1-aminoethyl)-N-(pyridin-4-yl)cyclohexanecarboxamide dihydrochloride
• Target: TGF-beta/Smad
• Solubility: Soluble in DMSO, not in water
• Storage: Desiccate at RT
• IUPAC Name: 4-[(1R)-1-aminoethyl]-N-pyridin-4-ylcyclohexane-1-carboxamide;dihydrochloride
• InChI: InChI=1S/C14H21N3O.2ClH/c1-10(15)11-2-4-12(5-3-11)14(18)17-13-6-8-16-9-7-13;;/h6-12H,2-5,15H2,1H3,(H,16,17,18);2*1H/t10-,11?,12?;;/m1../s1
• InChIKey: IDDDVXIUIXWAGJ-DDSAHXNVSA-N
• SMILES: C[C@H](C1CCC(CC1)C(=O)NC2=CC=NC=C2)N.Cl.Cl

Y-27632 dihydrochloride（Cat No.:I010113）is a selective inhibitor of Rho-associated protein kinase (ROCK), an enzyme involved in regulating various cellular processes, including cytoskeletal dynamics and cell migration. By inhibiting ROCK, Y-27632 promotes cell survival, enhances proliferation, and facilitates the dissociation of cells from the extracellular matrix, making it valuable in research related to stem cell biology and tissue engineering. It has also shown potential in various therapeutic applications, including cardiovascular diseases and neuroprotection. Its ability to modulate cell behavior makes Y-27632 a critical tool for studying cellular mechanisms and developing regenerative therapies.

Reference

1:Am J Respir Cell Mol Biol. 2014 Nov;51(5):701-8. doi: 10.1165/rcmb.2013-0484OC. Airway hyperresponsiveness induced by repeated esophageal infusion of HCl in guinea pigs.Cheng YM,Cao AL,Zheng JP,Wang HW,Sun YS,Liu CF,Zhang BB,Wang Y,Zhu SL,Wu DZ, PMID: 24828018 DOI: 10.1165/rcmb.2013-0484OC
Abstract: Gastroesophageal reflux is a common disorder closely related to chronic airway diseases, such as chronic cough, asthma, chronic bronchitis, and chronic obstructive disease. Indeed, gastroesophageal acid reflux into the respiratory tract causes bronchoconstriction, but the underlying mechanisms have still not been clarified. This study aimed to elucidate functional changes of bronchial smooth muscles (BSMs) isolated from guinea pigs in an animal model of gastroesophageal reflux. The marked airway inflammation, hyperresponsiveness and remodeling were observed after guinea pigs were exposed to intraesophageal HCl infusion for 14 days. In addition, contractile responses to acetylcholine (ACh), KCl, electrical field stimulation, and extracellular Ca(2+) were greater in guinea pigs infused with HCl compared with control groups. The L-type voltage-dependent Ca(2+) channels (L-VDCC) blocker, nicardipine, significantly inhibited ACh- and Ca(2+)-enhanced BSM contractions in guinea pigs infused with HCl. The Rho-kinase inhibitor, Y27632, attenuated ACh-enhanced BSM contractions in guinea pigs infused with HCl. Moreover, mRNA and protein expressions for muscarinic M2 and M3 receptors, RhoA, and L-VDCC in BSM were detected by real-time PCR and Western blot. Expressions of mRNA and protein for muscarinic M3 receptors, RhoA, and L-VDCC were greater than in BSM of HCl-infused guinea pigs, whereas levels of muscarinic M2 receptors were unchanged. We demonstrate that acid infusion to the lower esophagus and, subsequently, microaspiration into the respiratory tract in guinea pigs leads to airway hyperresponsiveness and overactive BSM. Functional and molecular results indicate that overactive BSM is the reason for enhancement of extracellular Ca(2+) influx via L-VDCC and Ca(2+) sensitization through Rho-kinase signaling.