Gedatolisib - CAS 1196160-78-3
Catalog number: 1196160-78-3
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Gedatolisib, also known as PKI-587 and PF-05212384, is an agent targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. Upon intravenous administration, PI3K/mTOR kinase inhibitor PKI-587 inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.
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white solid powder
PKI-587; PF-05212384; PF5212384; PF05212384; PF 05212384
Current Developer:
Pfizer Inc
1.A randomized phase II non-comparative study of PF-04691502 and gedatolisib (PF-05212384) in patients with recurrent endometrial cancer.
Del Campo JM1, Birrer M2, Davis C3, Fujiwara K4, Gollerkeri A5, Gore M6, Houk B7, Lau S8, Poveda A9, González-Martín A10, Muller C11, Muro K12, Pierce K13, Suzuki M14, Vermette J15, Oza A16. Gynecol Oncol. 2016 Apr 23. pii: S0090-8258(16)30151-2. doi: 10.1016/j.ygyno.2016.04.019. [Epub ahead of print]
OBJECTIVE: PF-04691502 and gedatolisib (PF-05212384) are potent, dual PI3K/mTOR inhibitors. This phase II study (B1271004) was conducted in patients with recurrent endometrial cancer following platinum-containing chemotherapy. The primary endpoint was to assess clinical benefit response (complete or partial response, or stable disease for ≥16weeks) following treatment with PF-04691502 or gedatolisib.
2.Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML.
Lindblad O1,2,3, Cordero E1, Puissant A4, Macaulay L1,2, Ramos A5, Kabir NN6, Sun J1,2, Vallon-Christersson J7, Haraldsson K7, Hemann MT5, Borg Å7, Levander F8, Stegmaier K4, Pietras K1, Rönnstrand L1,2, Kazi JU1,2,6. Oncogene. 2016 Mar 21. doi: 10.1038/onc.2016.41. [Epub ahead of print]
Therapy directed against oncogenic FLT3 has been shown to induce response in patients with acute myeloid leukemia (AML), but these responses are almost always transient. To address the mechanism of FLT3 inhibitor resistance, we generated two resistant AML cell lines by sustained treatment with the FLT3 inhibitor sorafenib. Parental cell lines carry the FLT3-ITD (tandem duplication) mutation and are highly responsive to FLT3 inhibitors, whereas resistant cell lines display resistance to multiple FLT3 inhibitors. Sanger sequencing and protein mass-spectrometry did not identify any acquired mutations in FLT3 in the resistant cells. Moreover, sorafenib treatment effectively blocked FLT3 activation in resistant cells, whereas it was unable to block colony formation or cell survival, suggesting that the resistant cells are no longer FLT3 dependent. Gene expression analysis of sensitive and resistant cell lines, as well as of blasts from patients with sorafenib-resistant AML, suggested an enrichment of the PI3K/mTOR pathway in the resistant phenotype, which was further supported by next-generation sequencing and phospho-specific-antibody array analysis.
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CAS 1196160-78-3 Gedatolisib

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