| Cas No.: | 152-11-4 |
| SMILES: | Cl.COC1=CC=C(CCN(CCCC(C2=CC=C(OC)C(OC)=C2)(C#N)C(C)C)C)C=C1OC |
| Formula: | C27H39ClN2O4 |
| M.Wt: | 491.06 |
| Purity: | >98% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Verapamil Hcl is an L-type calcium channel blocker of the phenylalkylamine class.in vitro: In the K562/ADR cellline, addition of verapamil to the culture medium (15 microM concentration) resulted in a 3-fold decrease in Pgp expression after 72 hr exposure. The combination of bortezomib and verapamil synergistically decreased the viability of myeloma cells by inducing cell death. Importantly, bortezomib-mediated activation of major UPR components was enhanced by verapamil. The combination of bortezomib and verapamilresulted in caspase activation followed by poly(ADP-ribose) polymerase cleavage, whereas nuclear factor kappaB (NF-kappaB) activity declined in myeloma cells. in vivo: Pretreatment with cadmium plusverapamil produced significant additive effects on ketamine-induced anesthesia (40.88 +/- 2.98 vs 70.32 +/- 4.64 min). In the acute stage (17 days after infection with maximal parasitemia), verapamil treatment not only decreased the incidence of myocardial disease (fibrosis and inflammation), but also protected myocardial beta-adrenergic adenylate cyclase activity. In addition, there was no increase in total body weight, which was regarded as an index of right-sided heart failure. In the subacute stage (30 to 60 days after infection), administration of verapamil continued to decrease myocardial disease and preserve beta-adrenergic adenylate cyclase activity. |

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