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Q94 hydrochloride
Axon 2055
- Parent CAS: 537009-12-4
Purity:
99%
- Soluble in DMSO
- MF: C21H17ClN2.HCl
- MW: 369.29
Description
Q94 hydrochloride is a PAR1/Gαq-selective allosteric inhibitor and negative allosteric modulator. It selectively disrupts PAR1 coupling to Gαq-dependent signaling rather than broadly blocking all PAR1 functions.
PAR1 is a thrombin-activated GPCR that can signal through multiple G proteins and β-arrestin pathways. Q94 is useful for studying biased or pathway-selective PAR1 pharmacology, especially Gαq-dependent signaling mechanisms.
Key Features
- PAR1/Gαq-selective allosteric inhibitor
- Negative allosteric modulator of PAR1 signaling
- Selectively blocks PAR1-Gαq interaction
- Useful for pathway-biased GPCR pharmacology
Applications
- PAR1 signaling assays
- Gαq pathway studies
- Thrombin receptor pharmacology
- Biased GPCR signaling research
More Information
| Parent CAS No. | 537009-12-4 |
|---|---|
| Chemical Name | 2-benzyl-1-(4-chlorobenzyl)-1H-benzo[d]imidazole hydrochloride |
| SMILES | C1(CC2=CC=CC=C2)N(CC2=CC=C(Cl)C=C2)C2=CC=CC=C2N=1.Cl |
| MFCD | N.A. |
| InChi | InChI=1S/C21H17ClN2.ClH/c22-18-12-10-17(11-13-18)15-24-20-9-5-4-8-19(20)23-21(24)14-16-6-2-1-3-7-16;/h1-13H,14-15H2;1H |
| InChiKey | WXIWQTVPWYFEHP-UHFFFAOYSA-N |
| CID | 16258217 |
| Short Description | PAR1 antagonist |
Q94 hydrochloride
PAR1/Gαq-selective allosteric inhibitor
Q94
PAR1
PAR1/Gαq-selective allosteric
Inhibitor
GPCR signaling
PAR1 signaling assays
Gαq pathway studies
Thrombin receptor pharmacology
Biased GPCR signaling research
GPCR pharmacology
receptor selectivity
signal transduction
receptor pharmacology
enzyme pharmacology
GPCR
CAS 537009-12-4
CAS 1052076-77-3
Axon Medchem
Axon 2055
Supplier
Vendor
References
- X Ding et al. Thrombin induces fibroblast CCL2/JE production and release via coupling of PAR1 to Gαq and cooperation between ERK1/2 and Rho kinase signaling pathways. Mol. Biol. Cell, 2008, 19(6), 2520-2533.
- S Asteriti et al. Modulation of PAR1 signalling by benzimidazole compounds. Br. J. Pharmacol. 2012, 167, 80–94.
- PF Mercer et al. Pulmonary Epithelium Is a Prominent Source of Proteinase-activated Receptor-1–inducible CCL2 in Pulmonary Fibrosis. Am. J. Resp. Critical Care Med. 2009, 179(5), 414-425.
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