Methods for cancer therapy
a cancer and cancer technology, applied in the field of cancer therapy, can solve the problems of inability of second-generation inhibitors to inhibit the most refractory bcr-abl, and the difficulty of overcoming acquired resistance to imatinib,
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example 1
[0097]A single-agent, open-label dose escalation and dose expansion Phase I study to assess the safety, preliminary efficacy, pharmacokinetic (PK) and pharmacodynamic (PD) properties of orally administered the compound of formula (I-A) in the TKI-resistant patients with chronic phase (CP) or accelerated phase (AP) CML.
[0098]Methods: the compound of formula (I-A) was administered orally once every other day (QOD) in 28-days cycles at 11 dose cohorts ranging from 1 mg to 60 mg. The eligible patients received treatments until disease progression or intolerable toxicities. The primary efficacy endpoint in the CML AP and CP patients, was complete hematological response (CHR) and major cytogenetic response (MCyR) respectively, MCyR includes partial cytogenetic response (PCyR) and complete cytogenetic response (CCyR). Blood samples were collected at various time points on Day 1-2 and Day 27-28 during cycle 1 for PK analyses. BCR-ABL inhibition was evaluated using tyrosine phosphorylation o...
example 2
[0167]Further Efficacy and Safety Results of Phase 1 Study of the compound of formula (I-A) in Patients with Resistant Chronic Myeloid Leukemia
[0168]The compound of formula (I-A) is designed for treatment of patients with chronic myeloid leukemia (CML) resistant to current TKI-therapies including those with T315I mutation. This experiment is focus on the efficacy and safety assessment of the compound of formula (I-A) in a relatively long term.
[0169]Methods:
[0170]An open-label, 3+3 dose escalation, phase 1 trial of the compound of formula (I-A) design to determine maximum tolerated dose (MTD) and identify dose-limiting toxicities (DLTs) in patients with chronic phase (CP / CML-CP) or accelerated phase (AP / CML-AP) CML resistant to or intolerant of ≥2 prior TKIs or patients with BCR-ABL T315I M after ≥1 prior TKI is ongoing. The compound of formula (I-A) was administered once every other day (QOD) in 28-day cycles at 11 dose cohorts ranging from 1 mg to 60 mg. The eligible patients recei...
example 3
[0179]In this experiment, BCR-ABL complex mutation cells were used to determine the inhibitory effect of the compound of the formula (I-A) and Ponatinib on the proliferation of BCR-ABL complex mutation cells. The experiment proved that the compound of the formula (I-A) was a potential effective medicament capable of overcoming the drug resistance of the Ponatinib. Ba / F3 cells stably expressing BCR-ABL (F359V, H396R, E255K, Y253H, T315I, F317L) mutations were provided by the Institute of Life and Health, Guangzhou Academy of Sciences.
[0180]1. The mutated Ba / F3 cell line stably expressing BCR-ABL (E255V, T315M, Y253H / E255V, Y253H / T315I, Y253H / F359V, T315I / F317L, F317L / F359V) mutation was constructed by electro-transformation method, the Ba / F3 cell line stably expressing the BCR-ABL (E255V / T315I, T315I / F359V) mutation was constructed by lentivirus infection method. Cell gene sequencing results confirmed that the BCR-ABL mutant gene was integrated into the genome of Ba / F3 cells. Western...
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