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Asciminib, sold under the brand name Scemblix, is a medication used to treat Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML). Asciminib is a protein kinase inhibitor.
Read the full article on WikipediaChronic Myeloid Leukaemia (CML) Clinical criteria: Treatment Phase: Initial PBS-subsidised treatment for patients without T315I mutation The treatment must be the sole PBS-subsidised therapy for this condition, AND The condition must not be in the blast phase, AND The treatment must not exceed a total maximum of 18 months of therapy with PBS-subsidised treatment with a tyrosine kinase inhibitor for this condition under this restriction, AND The condition must be expressing the Philadelphia chromosome confirmed through cytogenetic analysis; OR The condition must have the transcript BCR-ABL tyrosine kinase confirmed through quantitative polymerase chain reaction (PCR), AND Patient must have failed an adequate trial of at least two tyrosine kinase inhibitors; OR Patient must have experienced intolerance, not failure to respond, to at least two tyrosine kinase inhibitors; OR Patient must have failed an adequate trial of at least one tyrosine kinase inhibitor with intolerance to at least another tyrosine kinase inhibitor. Failure of an adequate trial of a tyrosine kinase inhibitor is defined as: 1. Lack of response defined as either: (i) failure to achieve a haematological response after a minimum of 3 months therapy; or (ii) failure to achieve any cytogenetic response after a minimum of 6 months therapy as demonstrated on bone marrow biopsy by presence of greater than 95% Philadelphia chromosome positive (Ph+) cells; or (iii) failure to achieve or maintain a major cytogenetic response or a peripheral blood BCR-ABL level of less than 1% after a minimum of 12 months therapy; OR 2. Loss of a previously documented major cytogenetic response (demonstrated by the presence of greater than 35% Ph+ cells on bone marrow biopsy), during ongoing tyrosine kinase inhibitor (TKI) therapy; OR 3. Loss of a previously demonstrated molecular response (demonstrated by peripheral blood BCR-ABL levels increasing consecutively in value by at least 5 fold to a level of greater than 0.1% confirmed on a subsequent test), during ongoing tyrosine kinase inhibitor (TKI) therapy; OR 4. Development of accelerated phase in a patient previously prescribed a TKI inhibitor for any phase of chronic myeloid leukaemia; OR 5. Disease progression (defined as a greater than or equal to 50% increase in peripheral white blood cell count, blast count, basophils or platelets) during TKI therapy in patients with accelerated phase chronic myeloid leukaemia. Accelerated phase is defined by the presence of 1 or more of the following: 1. Percentage of blasts in the peripheral blood or bone marrow greater than or equal to 15% but less than 30%; or 2. Percentage of blasts plus promyelocytes in the peripheral blood or bone marrow greater than or equal to 30%, provided that blast count is less than 30%; or 3. Peripheral basophils greater than or equal to 20%; or 4. Progressive splenomegaly to a size greater than or equal to 10 cm below the left costal margin to be confirmed on 2 occasions at least 4 weeks apart, or a greater than or equal to 50% increase in size below the left costal margin over 4 weeks; or 5. Karyotypic evolution (chromosomal abnormalities in addition to a single Philadelphia chromosome).
“Asciminib is described as a "STAMP inhibitor," which means "specifically targeting the ABL myristoyl pocket." The wild-type ABL has a myristoylated N-terminus, which binds to an allosteric site, but the ABL fusion protein does not have the myristoylated domain. In the wild-type protein, when myristoylated N-terminus binds to the allosteric site, the kinase has reduced activity. Since the mutant fusion protein does not have the myristoylated N-terminus domain, it is not subject to this form of regulation, and thus the fusion protein is constitutively active. Asciminib binds to the allosteric site, resulting in an inhibition of bcr-abl activity.”
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