I-3344 INK128, Free Base, >99%

Synonyms : [MLN0128] [Sapanisertib]

  • Size
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  • 25 mg
  • 155
  • 143
  • 128
  • 20,300
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  • In stock
  • 50 mg
  • 236
  • 218
  • 195
  • 31,000
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  • In stock
  • 100 mg
  • 418
  • 386
  • 346
  • 54,800
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  • 200 mg
  • 633
  • 584
  • 525
  • 83,000
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  • 300 mg
  • 864
  • 798
  • 717
  • 113,300
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  • 500 mg
  • 1,245
  • 1,150
  • 1,033
  • 163,300
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  • 1 g
  • 1,930
  • 1,783
  • 1,601
  • 253,200
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  • M.W. 309.33
  • C15H15N7O
  • [1224844-38-5]

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  • INK128 is a potent mTOR kinase inhibitor with a Ki of 1.4 nM. It had therapeutic benefit for prostate cancer metastasis. Hsieh A.C., et al. "The translational landscape of mTOR signalling steers cancer initiation and metastasis." Nature 485: 55-61 (2012).
  • INK128 potently blocked cell proliferation in various breast cancer cell lines harboring PIK3CA (IC50 = 1.5-53 nM), PTEN (IC50 = 1-149 nM), KRAS and/or BRAF mutations (IC50 = 13-162 nM), and in human endothelial cells (IC50 = 33-40 nM) in vitro. In vivo, INK128 suppressed primary tumor growth significantly in both non-VEGF and VEGF-driven MCF-7 xenograft models. Gökmen-Polar Y., et al. "Investigational drug MLN0128, a novel TORC1/2 inhibitor, demonstrates potent oral antitumor activity in human breast cancer xenograft models." Breast Cancer Res. Treat. 136: 673-682 (2012).
  • INK128 inhibited proliferation of B-cell acute lymphoblastic leukemia (B-ALL) cell lines in vitro and suppressed colony formation by primary human leukemia cells from adult and pediatric B-ALL patients. INK128 enhanced the efficacy of dasatinib in Philadelphia Chromosome-positive (Ph+) specimens. In a syngeneic mouse model of lymphoid BCR-ABL+ disease, INK128 rapidly cleared leukemic outgrowth. In non-Ph+, B-ALL xenografts, INK128 had a cytostatic effect. Janes M.R., et al. "Efficacy of the investigational mTOR kinase inhibitor MLN0128/INK128 in models of B-cell acute lymphoblastic leukemia." Leukemia 27: 586-594 (2013).
  • The addition of lapatinib to INK-128 treatment resulted in inhibition of both PI3K/Akt/mTOR and ERK pathways and prevented both HER2 and HER3 phosphorylation induced by INK-128. This dual blockade demonstrated antitumor activity in preclinical models of breast cancer resistant to anti-HER2 therapy. García-García C., et al. "Dual mTORC1/2 and HER2 blockade results in antitumor activity in preclinical models of breast cancer resistant to anti-HER2 therapy." Clin. Cancer Res. 18: 2603-2612 (2012).
  • Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use
  • Not available in some countries; not available to some institutions; not available for some uses.
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