Q94 hydrochloride

Negative allosteric modulator at PAR1 receptor CAS# 1052076-77-3

Q94 hydrochloride

Catalog No. BCC6281----Order now to get a substantial discount!

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Chemical structure

Q94 hydrochloride

3D structure

Chemical Properties of Q94 hydrochloride

Cas No. 1052076-77-3 SDF Download SDF
PubChem ID 16258217 Appearance Powder
Formula C21H18Cl2N2 M.Wt 369.29
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 50 mM in DMSO and to 50 mM in ethanol
Chemical Name 2-benzyl-1-[(4-chlorophenyl)methyl]benzimidazole;hydrochloride
SMILES C1=CC=C(C=C1)CC2=NC3=CC=CC=C3N2CC4=CC=C(C=C4)Cl.Cl
Standard InChIKey WXIWQTVPWYFEHP-UHFFFAOYSA-N
Standard 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
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Q94 hydrochloride

DescriptionPAR1 negative allosteric modulator (IC50 = 916 nM); inhibits PAR1-Gαq interaction. Selective for PAR1 over PAR2. Blocks thrombin-induced intracellular calcium mobilization (IC50 = 10.3 nM), CCL2 expression, ERK1/2 and MLC phosphorylation, and IP3 production in cells.

Q94 hydrochloride Dilution Calculator

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Preparing Stock Solutions of Q94 hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.7079 mL 13.5395 mL 27.079 mL 54.158 mL 67.6975 mL
5 mM 0.5416 mL 2.7079 mL 5.4158 mL 10.8316 mL 13.5395 mL
10 mM 0.2708 mL 1.3539 mL 2.7079 mL 5.4158 mL 6.7697 mL
50 mM 0.0542 mL 0.2708 mL 0.5416 mL 1.0832 mL 1.3539 mL
100 mM 0.0271 mL 0.1354 mL 0.2708 mL 0.5416 mL 0.677 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Q94 hydrochloride

Unusual 4-arsonoanilinium cationic species in the hydrochloride salt of (4-aminophenyl)arsonic acid and formed in the reaction of the acid with copper(II) sulfate, copper(II) chloride and cadmium chloride.[Pubmed:28378716]

Acta Crystallogr C Struct Chem. 2017 Apr 1;73(Pt 4):325-330.

Structures having the unusual protonated 4-arsonoanilinium species, namely in the hydrochloride salt, C6H9AsNO3(+).Cl(-), (I), and the complex salts formed from the reaction of (4-aminophenyl)arsonic acid (p-arsanilic acid) with copper(II) sulfate, i.e. hexaaquacopper(II) bis(4-arsonoanilinium) disulfate dihydrate, (C6H9AsNO3)2[Cu(H2O)6](SO4)2.2H2O, (II), with copper(II) chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-mu-chlorido-cuprate(II)]], {(C6H9AsNO3)2[CuCl4]}n, (III), and with cadmium chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-mu-chlorido-cadmate(II)]], {(C6H9AsNO3)2[CdCl4]}n, (IV), have been determined. In (II), the two 4-arsonoanilinium cations are accompanied by [Cu(H2O)6](2+) cations with sulfate anions. In the isotypic complex salts (III) and (IV), they act as counter-cations to the {[CuCl4](2-)}n or {[CdCl4](2-)}n anionic polymer sheets, respectively. In (II), the [Cu(H2O)6](2+) ion sits on a crystallographic centre of symmetry and displays a slightly distorted octahedral coordination geometry. The asymmetric unit for (II) contains, in addition to half the [Cu(H2O)6](2+) ion, one 4-arsonoanilinium cation, a sulfate dianion and a solvent water molecule. Extensive O-H...O and N-H...O hydrogen bonds link all the species, giving an overall three-dimensional structure. In (III), four of the chloride ligands are related by inversion [Cu-Cl = 2.2826 (8) and 2.2990 (9) A], with the other two sites of the tetragonally distorted octahedral CuCl6 unit occupied by symmetry-generated Cl-atom donors [Cu-Cl = 2.9833 (9) A], forming a two-dimensional coordination polymer network substructure lying parallel to (001). In the crystal, the polymer layers are linked across [001] by a number of bridging hydrogen bonds involving N-H...Cl interactions from head-to-head-linked As-O-H...O 4-arsonoanilinium cations. A three-dimensional network structure is formed. Cd(II) compound (IV) is isotypic with Cu(II) complex (III), but with the central CdCl6 complex repeat unit having a more regular M-Cl bond-length range [2.5232 (12)-2.6931 (10) A] compared to that in (III). This series of compounds represents the first reported crystal structures having the protonated 4-arsonoanilinium species.

Lens opacities in children using methylphenidate hydrochloride.[Pubmed:28376677]

Cutan Ocul Toxicol. 2017 Dec;36(4):362-365.

PURPOSE: To assess clinical findings of eye examination in children having attention deficit hyperactivity disorder (ADHD) administered with methylphenidate hydrochloride. METHODS: Fifty-seven consecutive patients diagnosed of ADHD and administered with oral methylphenidate hydrochloride treatment for at least one year were involved in this study (Group 1). Sixty healthy subjects (Group 2) having demographic features similar to group 1 were involved as a control group. All patients underwent detailed ophthalmological examination. RESULTS: One hundred and seventeen consecutive subjects with a mean age of 11.2 +/- 2.4 years (7-18 years) were enrolled. Fifty-seven consecutive patient (32 males, 25 females) under oral methylphenidate hydrochloride treatment (Group 1) and 60 healthy control subjects (30 males, 30 females) (Group 2)) were recruited for this prospective study. The mean methylphenidate hydrochloride dosage was 0.9 +/- 0.1 mg/kg/day and the mean duration of methylphenidate hydrochloride usage was for 2.73 +/- 0.73 years (1-7 years). High intraocular pressure was not observed in any of the patients in our study. We detected lens opacities in five eyes of five patients in group 1 (p = 0.019). The patient with the highest degree of cataract formation had been using MPH for 84 months and this patient's cataract score was P4. CONCLUSION: Long-term use of methylphenidate may cause lens opacities. In particular, patients who have been using methylphenidate for more than two years should go for regular eye examination.

Biophysical Study on the Interaction between Eperisone Hydrochloride and Human Serum Albumin Using Spectroscopic, Calorimetric, and Molecular Docking Analyses.[Pubmed:28380300]

Mol Pharm. 2017 May 1;14(5):1656-1665.

Eperisone hydrochloride (EH) is widely used as a muscle relaxant for patients with muscular contracture, low back pain, or spasticity. Human serum albumin (HSA) is a highly soluble negatively charged, endogenous and abundant plasma protein ascribed with the ligand binding and transport properties. The current study was undertaken to explore the interaction between EH and the serum transport protein, HSA. Study of the interaction between HSA and EH was carried by UV-vis, fluorescence quenching, circular dichroism (CD), Fourier transform infrared (FTIR) spectroscopy, Forster's resonance energy transfer, isothermal titration calorimetry and differential scanning calorimetry. Tryptophan fluorescence intensity of HSA was strongly quenched by EH. The binding constants (Kb) were obtained by fluorescence quenching, and results show that the HSA-EH interaction revealed a static mode of quenching with binding constant Kb approximately 10(4) reflecting high affinity of EH for HSA. The negative DeltaG degrees value for binding indicated that HSA-EH interaction was a spontaneous process. Thermodynamic analysis shows HSA-EH complex formation occurs primarily due to hydrophobic interactions, and hydrogen bonds were facilitated at the binding of EH. EH binding induces alpha-helix of HSA as obtained by far-UV CD and FTIR spectroscopy. In addition, the distance between EH (acceptor) and Trp residue of HSA (donor) was calculated 2.18 nm using Forster's resonance energy transfer theory. Furthermore, molecular docking results revealed EH binds with HSA, and binding site was positioned in Sudlow Site I of HSA (subdomain IIA). This work provides a useful experimental strategy for studying the interaction of myorelaxant with HSA, helping to understand the activity and mechanism of drug binding.

Fabrication yields of serially harvested calf-fed Holstein steers fed zilpaterol hydrochloride.[Pubmed:28380524]

J Anim Sci. 2017 Mar;95(3):1209-1218.

Holstein steers ( = 110) were fed zilpaterol hydrochloride (ZH) for 0 or 20 d before slaughter during a 280-d serial harvest study. Cattle were harvested every 28 d beginning at 254 d on feed (DOF) and concluding at 534 DOF. After slaughter, carcasses were chilled for 48 h and then fabricated into boneless closely trimmed or denuded subprimals, lean trim, trimmable fat, and bone. Inclusion of ZH increased cold side weight (CSW) by 10.3 kg ( < 0.01; 212.7 vs. 202.4 kg [SEM 1.96]) and saleable yield by 10.4 kg ( < 0.01; 131.9 vs. 121.5 kg [SEM 1.16]) in calf-fed Holstein steer carcasses. Additionally, saleable yield as a percentage of CSW increased (

Modulation of PAR(1) signalling by benzimidazole compounds.[Pubmed:22519452]

Br J Pharmacol. 2012 Sep;167(1):80-94.

BACKGROUND AND PURPOSE: Recently, a small molecule (Q94) was reported to selectively block PAR(1) /Galpha(q) interaction and signalling. Here, we describe the pharmacological properties of Q94 and two analogues that share its benzimidazole scaffold (Q109, Q89). Q109 presents a modest variation from Q94 in the substituent group at the 2-position, while Q89 has quite different groups at the 1- and 2-positions. EXPERIMENTAL APPROACH: Using human microvascular endothelial cells, we examined intracellular Ca(2+) mobilization and inositol 1,4,5-trisphosphate accumulation as well as isoprenaline- or forskolin-stimulated cAMP production in response to thrombin. KEY RESULTS: Q89 (10 microM) produced a leftward shift in the thrombin-mediated intracellular Ca(2+) mobilization concentration-response curve while having no effect on the E(max) . Both Q94 (10 microM) and Q109 (10 microM) reduced intracellular Ca(2+) mobilization, leading to a decrease in E(max) and an increase in EC(50) values. Experiments utilizing receptor-specific activating peptides confirmed that Q94 and Q109 were selective for PAR(1) as they did not alter the Ca(2+) response mediated by a PAR(2) activating peptide. Consistent with our Ca(2+) results, micromolar concentrations of either Q94 or Q109 significantly reduced thrombin-induced inositol 1,4,5-trisphosphate production. Neither Q94 nor Q109 diminished the inhibitory effects of thrombin on cAMP production, indicating they inhibit signalling selectively through the G(q) pathway. Our results also suggest the 1,2-disubstituted benzimidazole derivatives act as 'allosteric agonists' of PAR(1) . CONCLUSIONS AND IMPLICATIONS: The Q94 and Q109 benzimidazole derivatives represent a novel scaffold for the development of new PAR(1) inhibitors and provide a starting point to develop dual signalling pathway-selective positive/negative modulators of PAR(1) .

Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury.[Pubmed:19652365]

J Clin Invest. 2009 Sep;119(9):2550-63.

Uncontrolled activation of the coagulation cascade contributes to the pathophysiology of several conditions, including acute and chronic lung diseases. Coagulation zymogens are considered to be largely derived from the circulation and locally activated in response to tissue injury and microvascular leak. Here we report that expression of coagulation factor X (FX) is locally increased in human and murine fibrotic lung tissue, with marked immunostaining associated with bronchial and alveolar epithelia. FXa was a potent inducer of the myofibroblast differentiation program in cultured primary human adult lung fibroblasts via TGF-beta activation that was mediated by proteinase-activated receptor-1 (PAR1) and integrin alphavbeta5. PAR1, alphavbeta5, and alpha-SMA colocalized to fibrotic foci in lung biopsy specimens from individuals with idiopathic pulmonary fibrosis. Moreover, we demonstrated a causal link between FXa and fibrosis development by showing that a direct FXa inhibitor attenuated bleomycin-induced pulmonary fibrosis in mice. These data support what we believe to be a novel pathogenetic mechanism by which FXa, a central proteinase of the coagulation cascade, is locally expressed and drives the fibrotic response to lung injury. These findings herald a shift in our understanding of the origins of excessive procoagulant activity and place PAR1 central to the cross-talk between local procoagulant signaling and tissue remodeling.

Thrombin induces fibroblast CCL2/JE production and release via coupling of PAR1 to Galphaq and cooperation between ERK1/2 and Rho kinase signaling pathways.[Pubmed:18353977]

Mol Biol Cell. 2008 Jun;19(6):2520-33.

Uncontrolled activation of the coagulation cascade after tissue injury has been implicated in both inflammation and tissue fibrosis. Thrombin exerts pluripotent cellular effects via its high-affinity receptor, proteinase-activated receptor-1 (PAR(1)) and signaling via Galpha(i/o), Galpha(q), or Galpha(12/13). Activation of PAR(1) on fibroblasts, a key effector cell in fibrosis, results in the induction of several mediators, including the potent monocyte and fibrocyte chemoattractant CCL2. The aim of this study was to identify the G protein and signaling pathway involved in PAR(1)-mediated CCL2 production and release. Using a novel PAR(1) antagonist that blocks the interaction between PAR(1) and Galpha(q), we report for the first time that PAR(1) coupling to Galpha(q) is essential for thrombin-induced CCL2 gene expression and protein release in murine lung fibroblasts. We further demonstrate that these effects are mediated via the cooperation between ERK1/2 and Rho kinase signaling pathways: a calcium-independent protein kinase C (PKC), c-Raf, and ERK1/2 pathway was found to mediate PAR(1)-induced CCL2 gene transcription, whereas a phospholipase C, calcium-dependent PKC, and Rho kinase pathway influences CCL2 protein release. We propose that targeting the interaction between PAR(1) and Galpha(q) may allow us to selectively interfere with PAR(1) proinflammatory and profibrotic signaling, while preserving the essential role of other PAR(1)-mediated cellular responses.

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