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GSK690693

Catalog No.S1113 1 Review(s)
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GSK690693 Chemical Structure

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Biological Activity

GSK690693 is an aminofurazan-derived,novel ATP-competitive, low-nanomolar pan-Akt kinase inhibitor. It is selective for the Akt isoforms(inhibits Akt kinases 1, 2, and 3 with IC50 values of 2, 13, and 9 nM respectively)versus the majority of kinases in other families; however, it does inhibit additional members of the AGC kinase family. [1,2]

GSK690693 inhibited proliferation and induced apoptosis in a subset of tumor cells with potency consistent with intracellular inhibition of Akt kinase activity. [1]

Daily administration of GSK690693 produced significant antitumor activity in mice bearing established human SKOV-3 ovarian, LNCaP prostate, and BT474 and HCC-1954 breast carcinoma xenografts. [1]

References on GSK690693
  • [1] Cancer Res 2008;68:2366-2374
  • [2] J. Med. Chem 2008;51: 5663–5679
Molecular Weight (WM): 425.48
Formula:

C21H27N7O3

CAS No.: 937174-76-0
Synonyms:
N/A
Dissolve in (25°C): DMSO ≥39mg/mL 
Water <1mg/mL 
Ethanol <1mg/mL 
Storage: 2 years-20°CPowder
1 week-4°Cin DMSO
1 month-80°in DMSO

Quality Control & MSDS

View current batch:
COA H-NMR HPLC COA COA H-NMR HPLC COA H-NMR HPLC COA H-NMR HPLC
Notes:

Related Inhibitors

Related Antibodies

Recommended Screening Libraries

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Average Customer Review

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  • Click to enlarge
    Cell growth of sensitive (DLD1 and U87) and multi-drug resistant (DLD1-TxR and U87-TxR) cells assessed after 72 h of GSK690693 treatment. GSK690693 efficacy decreased in DLD1-TxR in comparison to its sensitive counterpart - DLD1. Colorectal carcinoma cell line (DLD1) possesses mutated p53, while its resistant counterpart (DLD1-TxR) additionally acquired the LOH in PTEN gene during the course of resistance induction. However, concentration-dependent cell growth inhibition induced by GSK690693 does not differ between sensitive (U87) and resistant (U87-TxR) glioblastoma cell lines. Both, U87 and U87-TxR have wt-p53 and PTEN-null. The results were obtained by the Sulforhodamine B assay. All values represent average ± SD obtained from two independent experiments, n = 5.
  • Cell growth of sensitive (DLD1 and U87) and multi-drug resistant (DLD1-TxR and U87-TxR) cells assessed after 72 h of GSK690693 treatment. GSK690693 efficacy decreased in DLD1-TxR in comparison to its sensitive counterpart - DLD1. Colorectal carcinoma cell line (DLD1) possesses mutated p53, while its resistant counterpart (DLD1-TxR) additionally acquired the LOH in PTEN gene during the course of resistance induction. However, concentration-dependent cell growth inhibition induced by GSK690693 does not differ between sensitive (U87) and resistant (U87-TxR) glioblastoma cell lines. Both, U87 and U87-TxR have wt-p53 and PTEN-null. The results were obtained by the Sulforhodamine B assay. All values represent average ± SD obtained from two independent experiments, n = 5.
  • Data independently produced by Dr Milica Pesic of Institute for Biological Research
    GSK690693 purchased from Selleck

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Cell growth of sensitive (DLD1 and U87) and multi-drug resistant (DLD1-TxR and U87-TxR) cells assessed after 72 h of GSK690693 treatment. GSK690693 efficacy decreased in DLD1-TxR in comparison to its sensitive counterpart - DLD1. Colorectal carcinoma cell line (DLD1) possesses mutated p53, while its resistant counterpart (DLD1-TxR) additionally acquired the LOH in PTEN gene during the course of resistance induction. However, concentration-dependent cell growth inhibition induced by GSK690693 does not differ between sensitive (U87) and resistant (U87-TxR) glioblastoma cell lines. Both, U87 and U87-TxR have wt-p53 and PTEN-null. The results were obtained by the Sulforhodamine B assay. All values represent average ± SD obtained from two independent experiments, n = 5.

Data independently produced by Dr Milica Pesic of Institute for Biological Research

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