Cinaciguat hydrochloride

Cinaciguat hydrochloride is a potent soluble guanylate cyclase (GC) activator with EC50 of 15 nM in platelets.

Product information

CAS Number: 646995-35-9

Molecular Weight: 602.16

Formula: C36H40ClNO5

Chemical Name: 4-{[(4-carboxybutyl)[2-(2-{[4-(2-phenylethyl)phenyl]methoxy}phenyl)ethyl]amino]methyl}benzoic acid; chlorohydrogen

Smiles: Cl.OC(=O)CCCCN(CC1C=CC(=CC=1)C(O)=O)CCC1=CC=CC=C1OCC1C=CC(CCC2C=CC=CC=2)=CC=1

InChiKey: LLHMBJOVHATVSP-UHFFFAOYSA-N

InChi: InChI=1S/C36H39NO5.ClH/c38-35(39)12-6-7-24-37(26-30-19-21-33(22-20-30)36(40)41)25-23-32-10-4-5-11-34(32)42-27-31-17-15-29(16-18-31)14-13-28-8-2-1-3-9-28;/h1-5,8-11,15-22H,6-7,12-14,23-27H2,(H,38,39)(H,40,41);1H

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 110 mg/mL (182.68 mM; Need ultrasonic).

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

In platelets, Cinaciguat (BAY 58-2667) is a potent GC activator (EC50 15 nM) but the maximum effect is only about 1% of that achievable with NO. Concentration-response curves for Cinaciguat are constructed after 1 min exposure in the presence of sildenafil. Without ODQ, the EC50 is 18 nM, and in the presence of ODQ the potency of Cinaciguat is not significantly different, the EC50 being 13 nM. The potency of Cinaciguat in platelets (EC50 15 nM) is very similar to estimates made on purified recombinant GC. Cinaciguat at a maximally effective concentration of 1 μM stimulates control GC activity to about 25% of that observed with NO and, contrasting with the stimulation by NO, this level of activity remained constant as the proportion of ODQ-pretreated GC is increased.

In Vivo:

Administration of Cinaciguat decreased BP and increased HR in both apo-sGC mice and WT mice. In fact, the BP-lowering effect of Cinaciguat in apo-sGC mice is significantly greater and longer lasting than in WT mice. In addition, Cinaciguat decreased BP in apo-sGC mice at concentrations that did not affect BP in WT mice. Furthermore, the IC50 values for Cinaciguat-induced ex vivorelaxation of precontracted aortas are threefold lower in apo-sGC mice than in WT mice (IC50=0.2 nM and 0.7 nM, respectively). Together, our results suggest that sGC activators like Cinaciguat but not sGC stimulators like BAY 41-2272 activate apo-sGC. In addition, the observation that Cinaciguat can modulate vasorelaxation and BP in WT mice suggests that even in healthy mice, a subset of the available sGC pool is haem-free and responsive to sGC activators.

Products are for research use only. Not for human use.