SAR7334 - CAS 1333210-07-3
Catalog number: B0084-474482
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C21H22ClN3O
Molecular Weight:
367.87
COA:
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Targets:
TRP Channel
Description:
SAR7334, a TRPC6 inhibitor, could be valuable in studying sorts of diseases related to TRPC.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-474482 5 mg $199 In stock
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Purity:
98%
Appearance:
Powder
Synonyms:
SAR7334; CPA1588; SAR 7334; CPA 1588; SAR-7334; CPA-1588; 4-(((1R,2R)-2-((R)-3-aminopiperidin-1-yl)-2,3-dihydro-1H-inden-1-yl)oxy)-3-chlorobenzonitrile; 1333207-63-8; 1333210-07-3; C21H22ClN3O
Solubility:
10 mM in DMSO
Storage:
-20ºC Freeze
MSDS:
Inquire
Application:
SAR7334 is a TRPC6 inhibitor that could be valuable in studying sorts of diseases related to TRPC.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Milligrams-Grams
InChIKey:
RLKRLNQEXBPQGQ-OZOXKJRCSA-N
InChI:
InChI=1S/C21H22ClN3O/c22-18-10-14(12-23)7-8-20(18)26-21-17-6-2-1-4-15(17)11-19(21)25-9-3-5-16(24)13-25/h1-2,4,6-8,10,16,19,21H,3,5,9,11,13,24H2/t16-,19-,21-/m1/s1
Canonical SMILES:
C1CC(CN(C1)C2CC3=CC=CC=C3C2OC4=C(C=C(C=C4)C#N)Cl)N
1.The Role of Angiotensin II in Glomerular Volume Dynamics and Podocyte Calcium Handling.
Ilatovskaya DV;Palygin O;Levchenko V;Endres BT;Staruschenko A Sci Rep. 2017 Mar 22;7(1):299. doi: 10.1038/s41598-017-00406-2.
Podocytes are becoming a primary focus of research efforts due to their association with progressive glomeruli damage in disease states. Loss of podocytes can occur as a result of excessive intracellular calcium influx, and we have previously shown that angiotensin II (Ang II) via canonical transient receptor potential 6 (TRPC6) channels caused increased intracellular Ca;2+; flux in podocytes. We showed here with patch-clamp electrophysiology that Ang II activates TRPC channels; then using confocal calcium imaging we demonstrated that Ang II-dependent stimulation of Ca;2+; influx in the podocytes is precluded by blocking either AT;1; or AT;2; receptors (ATRs). Application of Ang(1-7) had no effect on intracellular calcium. Ang II-induced calcium flux was decreased upon inhibition of TRPC channels with SAR7334, SKF 96365, clemizole hydrochloride and La;3+;, but not ML204. Using a novel 3D whole-glomerulus imaging ex vivo assay, we revealed the involvement of both ATRs in controlling glomerular permeability; additionally, using specific inhibitors and activators of TRPC6, we showed that these channels are implicated in the regulation of glomerular volume dynamics. Therefore, we provide evidence demonstrating the critical role of Ang II/TRPC6 axis in the control of glomeruli function, which is likely important for the development of glomerular diseases.
2.Ribemansides A and B, TRPC6 Inhibitors from Ribes manshuricum That Suppress TGF-β1-Induced Fibrogenesis in HK-2 Cells.
Zhou B;Wang Y;Zhang C;Yang G;Zhang F;Yu B;Chai C;Cao Z J Nat Prod. 2018 Apr 27;81(4):913-917. doi: 10.1021/acs.jnatprod.7b01037. Epub 2018 Feb 22.
Two new acylated β-hydroxynitrile glycosides, ribemansides A (1) and B (2), were isolated from the aerial parts of Ribes manshuricum. Their structures were elucidated by comprehensive spectroscopic analysis. Ribemansides A and B inhibited transforming growth factor β1 (TGF-β1)-induced expression of α-smooth muscle actin, fibronectin release, and changes in cell morphology in the human proximal tubular epithelial cell line (human kidney-2, HK-2). Further biological evaluation demonstrated that both 1 and 2 inhibit the activity of canonical transient receptor potential cation channel 6 (TRPC6), with IC;50; values of 24.5 and 25.6 μM, respectively. The antifibrogenic effect of these compounds appears to be mediated through TRPC6 inhibition, since the TRPC6 inhibitor, SAR7334, also suppressed TGF-β1-induced fibrogenesis in HK-2 cells.
3.Pharmacological Characterization of the Native Store-Operated Calcium Channels of Cortical Neurons from Embryonic Mouse Brain.
Chauvet S;Jarvis L;Chevallet M;Shrestha N;Groschner K;Bouron A Front Pharmacol. 2016 Dec 12;7:486. doi: 10.3389/fphar.2016.00486. eCollection 2016.
In the murine brain, the first post-mitotic cortical neurons formed during embryogenesis express store-operated channels (SOCs) sensitive to Pyr3, initially proposed as a blocker of the transient receptor potential channel of C type 3 (TRPC3 channel). However, Pyr3 does not discriminate between Orai and TRPC3 channels, questioning the contribution of TRPC3 in SOCs. This study was undertaken to clarify the molecular identity and the pharmacological profile of native SOCs from E13 cortical neurons. The mRNA expression of STIM1-2 and Orai1-3 was assessed by quantitative reverse transcription polymerase chain reaction. E13 cortical neurons expressed STIM1-2 mRNAs, with STIM2 being the predominant isoform. Only transcripts of Orai2 were found but no Orai1 and Orai3 mRNAs. Blockers of Orai and TRPC channels (Pyr6, Pyr10, EVP4593, SAR7334, and GSK-7975A) were used to further characterize the endogenous SOCs. Their activity was recorded using the fluorescent Ca;2+; probe Fluo-4. Cortical SOCs were sensitive to the Orai blockers Pyr6 and GSK-7975A, as well as to EVP4593, zinc, copper, and gadolinium ions, the latter one being the most potent SOCs blocker tested (IC;50; ∼10 nM). SOCs were insensitive to the TRPC channel blockers Pyr10 and SAR7334.
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