It is a highly potent of both BCR-ABL and Src kinases in sub-nanomolar concentrations, and serves as a polypharmacological dual inhibitor, thus relaxing its structural binding specificity to ABL and increasing tolerance to point amino acid mutations that would otherwise confer resistance to other kinase inhibitors; BMS-354825's characteristics allow it to override the M244V, G250E, Q252H, Q252R, Y253F, Y253H, E255K, E255V, F317L, M351T, E355G, F359V, H396R, and F486S mutations in ABL that otherwise confer resistance to imantinib, thus demonstrating its clinical relevance.
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rdf:type
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rdfs:label
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rdfs:comment
| - It is a highly potent of both BCR-ABL and Src kinases in sub-nanomolar concentrations, and serves as a polypharmacological dual inhibitor, thus relaxing its structural binding specificity to ABL and increasing tolerance to point amino acid mutations that would otherwise confer resistance to other kinase inhibitors; BMS-354825's characteristics allow it to override the M244V, G250E, Q252H, Q252R, Y253F, Y253H, E255K, E255V, F317L, M351T, E355G, F359V, H396R, and F486S mutations in ABL that otherwise confer resistance to imantinib, thus demonstrating its clinical relevance.
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side
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dbkwik:halo-fanon/...iPageUsesTemplate
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dbkwik:halofanon/p...iPageUsesTemplate
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Molweight
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Solubility
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Name
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Chemformula
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Mechanism
| - *BCR-ABL inhibitor, IC50 < 1.0 nM
*Src inhibitor, IC50 = 0.50 nM
*Lck inhibitor, IC50 = 0.40 nM
*Yes inhibitor, IC50 = 0.50 nM
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Clinuse
| - Chronic myelogenous leukemia anticancer drug
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Bioavail
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Marketed
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IUPAC name
| - N--2-thiazole-5-carboxamide
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Halflife
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Legal
| - Approved for clinical usage by the UNSC Medical Corps
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Route
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abstract
| - It is a highly potent of both BCR-ABL and Src kinases in sub-nanomolar concentrations, and serves as a polypharmacological dual inhibitor, thus relaxing its structural binding specificity to ABL and increasing tolerance to point amino acid mutations that would otherwise confer resistance to other kinase inhibitors; BMS-354825's characteristics allow it to override the M244V, G250E, Q252H, Q252R, Y253F, Y253H, E255K, E255V, F317L, M351T, E355G, F359V, H396R, and F486S mutations in ABL that otherwise confer resistance to imantinib, thus demonstrating its clinical relevance.
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