SKF-96365

SKF-96365 is a blocker of calcium store-operated calcium influx (SOCE) and transient receptor potential channels (TRPC) . SKF-96365 reduces the increase in intracellular calcium concentration by blocking TRPC channels and SOCE. SKF-96365 enhances the reverse operation of Na⁺/Ca²⁺ exchanger (NCX) (Ca²⁺ influx) in glioblastoma, leading to intracellular calcium overload and cytotoxicity. SKF-96365 inhibits the CaMKIIγ/AKT pathway and simultaneously induces apoptosis and cell protective autophagy in colorectal cancer cells. SKF-96365 can be used in calcium signaling and cancer research[1][2][3][4].

Product Specifications

CAS Number

[162849-90-3]

UNSPSC

12352005

Target

Akt; Apoptosis; Autophagy; Calcium Channel; CaMK; CRAC Channel; Na+/Ca2+ Exchanger; TRP Channel

Related Pathways

Apoptosis; Autophagy; Membrane Transporter/Ion Channel; Neuronal Signaling; PI3K/Akt/mTOR

Field of Research

Cancer; Neurological Disease

Smiles

COC1=CC=C(CCCOC(C2=CC=C(OC)C=C2)CN3C=CN=C3)C=C1

Molecular Formula

C22H26N2O3

Molecular Weight

366.45

References & Citations

[1]Jing Z, et al. SKF-96365 activates cytoprotective autophagy to delay apoptosis in colorectal cancer cells through inhibition of the calcium/CaMKIIγ/AKT-mediated pathway. Cancer Lett. 2016 Mar 28;372 (2) :226-38. |[2]Song M, Chen D, Yu SP. The TRPC channel blocker SKF 96365 inhibits glioblastoma cell growth by enhancing reverse mode of the Na (+) /Ca (2+) exchanger and increasing intracellular Ca (2+) . Br J Pharmacol. 2014 Jul;171 (14) :3432-47|[3]Chen T, et al. Protective effects of SKF-96365, a non-specific inhibitor of SOCE, against MPP+-induced cytotoxicity in PC12 cells: potential role of Homer1. PLoS One. 2013 Jan 31;8 (1) :e55601.|[4]Rae MG, Hilton J, Sharkey J. Putative TRP channel antagonists, SKF 96365, flufenamic acid and 2-APB, are non-competitive antagonists at recombinant human α1β2γ2 GABA (A) receptors. Neurochem Int. 2012 May;60 (6) :543-54.

Shipping Conditions

Room temperature

Scientific Category

Reference compound1

Clinical Information

No Development Reported

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