587852-28-6 Usage
Description
SMI-16a is a potent and selective Pim-1 kinase inhibitor with an IC50 value of 63 nM. It demonstrates high selectivity for Pim-1 over a panel of 60 kinases and effectively inhibits the phosphorylation of the Pim-1 target protein Bad in DU145-Pim cells. SMI-16a also shows significant growth inhibition in various cancer cell lines, including PC3, DU145, LNCaP, K562, and MV4-11. Additionally, it induces apoptosis and cell cycle arrest at the G1 phase in DU145 cells, making it a promising compound for cancer research and therapeutic development.
Uses
Used in Cancer Research:
SMI-16a is used as a research tool for studying the role of Pim-1 kinase in cancer cell growth and survival. Its high selectivity and potency make it an ideal candidate for investigating the molecular mechanisms underlying Pim-1-mediated oncogenic processes.
Used in Anticancer Drug Development:
SMI-16a is used as a lead compound in the development of novel anticancer therapeutics. Its ability to inhibit Pim-1 kinase, induce apoptosis, and cause cell cycle arrest in various cancer cell lines suggests its potential as a therapeutic agent for the treatment of multiple types of cancer.
Used in Drug Screening and Validation:
SMI-16a is used as a reference compound in high-throughput screening assays to identify new Pim-1 inhibitors with potential anticancer properties. Its well-characterized activity against Pim-1 kinase allows researchers to validate the efficacy and selectivity of newly discovered compounds.
Used in Combination Therapy Studies:
SMI-16a is used to explore the potential of combination therapies in cancer treatment. Its ability to induce apoptosis and cell cycle arrest in cancer cells can be combined with other targeted therapies or conventional chemotherapeutic agents to enhance treatment outcomes and overcome drug resistance.
Used in Molecular Mechanism Studies:
SMI-16a is used to investigate the molecular mechanisms underlying Pim-1-mediated oncogenic processes. By studying the effects of SMI-16a on various cancer cell lines, researchers can gain insights into the signaling pathways and cellular processes regulated by Pim-1 kinase, which may lead to the identification of new therapeutic targets in cancer.
Used in Preclinical Cancer Models:
SMI-16a is used in preclinical cancer models to evaluate its efficacy and safety as a potential anticancer agent. These studies help to determine the optimal dosing regimen, pharmacokinetics, and pharmacodynamics of SMI-16a, as well as its potential for adverse effects and drug-drug interactions.
Check Digit Verification of cas no
The CAS Registry Mumber 587852-28-6 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 5,8,7,8,5 and 2 respectively; the second part has 2 digits, 2 and 8 respectively.
Calculate Digit Verification of CAS Registry Number 587852-28:
(8*5)+(7*8)+(6*7)+(5*8)+(4*5)+(3*2)+(2*2)+(1*8)=216
216 % 10 = 6
So 587852-28-6 is a valid CAS Registry Number.
587852-28-6Relevant articles and documents
Composition for Distructing Microalgae
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Paragraph 0283-0288, (2017/04/12)
The present invention relates to a composition for disrupting microalgae. The composition for disrupting microalgae can suppress growth and proliferation of microalgae when treated in marine microalgae culture farms, areas where green or red tide takes pl
Structure-activity requirements for the antiproliferative effect of troglitazone derivatives mediated by depletion of intracellular calcium
Fan, Yun-Hua,Chen, Han,Natarajan, Amarnath,Guo, Yuhong,Harbinski, Fred,Iyasere, Julia,Christ, William,Aktas, Huseyin,Halperin, Jose A.
, p. 2547 - 2550 (2007/10/03)
Depletion of calcium from the endoplasmic reticulum has shown to affect protein synthesis and cell proliferation. The anticancer effect of troglitazone was reported to be mediated by depletion of intracellular calcium stores resulting in inhibition of translation initiation. The unsaturated form of troglitazone displays similar anticancer properties in vitro. In this letter, we report our findings on the minimum structural requirements for both compounds to retain their calcium release and antiproliferative activities.
