ABL1 pThr735 antibody Ab
- Known as:
- ABL1 pThr735 (anti-) Antibody
- Catalog number:
- 1488121
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- ABL1 pThr735 antibody
Related genes to: ABL1 pThr735 antibody Ab
- Gene:
- ABL1 NIH gene
- Name:
- ABL proto-oncogene 1, non-receptor tyrosine kinase
- Previous symbol:
- ABL
- Synonyms:
- JTK7, c-ABL, p150
- Chromosome:
- 9q34.12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ABL1 pThr735 antibody Ab
Related articles to: ABL1 pThr735 antibody Ab
- In chronic myeloid leukemia in chronic phase (CML-CP), BCR::ABL1 commonly leads to treatment resistance, worse patient outcomes, and limited subsequent treatment options. By targeting the ABL1 myristoyl pocket, asciminib maintains activity against BCR::ABL1. We report final long-term safety, tolerability, and efficacy results with asciminib in 48 patients with T315I-mutated CML-CP who received asciminib 200 mg twice daily in the phase 1, nonrandomized trial (NCT02081378). After a median exposure of 3.5 years, 52.1% of patients continued to receive asciminib via posttrial access. Of 45 evaluable patients, 24 (53.3%) achieved major molecular response (MMR); 20 of 24 maintained or deepened their response by the cutoff. The Kaplan-Meier estimated proportion of patients maintaining their first MMR for at least 144 weeks (2.8 years) was 86% (95% CI: 71.9-100.0%). The safety profile showed no new or worsening safety signals. With 1.4 years' additional exposure since the previous analysis, the incidence of grade ≥3 adverse events (AEs) (60.4%) did not increase. Four patients (8.3%) discontinued due to AEs. The exposure-adjusted incidence rate of first all-grade AOEs was 4.4 cases per 100 patient-years. With up to approximately 6 years of exposure, this final analysis confirms asciminib as a treatment option for patients with T315I-mutated CML-CP. - Source: PubMed
Publication date: 2026/07/16
Cortes Jorge ERea DelphineMauro Michael JHochhaus AndreasKim Dong-WookSasaki KojiLang FabianHeinrich Michael CBreccia MassimoDeininger MichaelGoh Yeow-TeeJanssen Jeroen J W MTalpaz MosheGómez García de Soria Vallele Coutre PhilippMahon Francois-XavierDeAngelo Daniel JDamon AndreaKapoor ShrutiSanchez-Olle GessamiHoch MatthiasAgrawal NithyaQuenet SaraHughes Timothy P - The BCR-ABL1 fusion gene is present in more than 95% of cases of chronic myeloid leukemia (CML), the disease in which it was first described. There are different BCR-ABL1 fusion transcripts depending on the location of the breakpoints during chromosomal translocation. Identifying these transcripts is important for treatment monitoring. The objective was to determine the frequency and distribution of BCR-ABL1 transcripts in African countries. - Source: PubMed
Publication date: 2026/07/14
Emeline Oloume MartinePieme AnatoleNgalle Cedric KekuineTapouli RansirTagny Claude Tayou - Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the BCR::ABL1 fusion oncogene. Asciminib, a first-in-class STAMP (Specifically Targeting the ABL Myristoyl Pocket) inhibitor, represents a novel therapeutic approach distinct from conventional ATP-competitive tyrosine kinase inhibitors (TKIs). This systematic review evaluated the efficacy and safety of asciminib as first-line therapy in patients with newly diagnosed chronic-phase CML. - Source: PubMed
Publication date: 2026/07/15
Han Jae JoonLee Jeong-OkKim Kyoung HaLee Sung-EunSohn Sang KyunJung Chul WonKim Hawk - Chronic myeloid leukemia (CML) is driven by the BCR::ABL1 fusion oncogene, with the p210 transcript accounting for over 98% of cases. RT-qPCR monitoring of the BCR::ABL1 fusion gene is the gold standard for detecting measurable residual disease (MRD) and guiding treatment-free remission (TFR) decisions. Most commercial assays are costly and limit accessibility in resource-constrained settings. We aimed to develop and validate an in-house one-step RT-qPCR assay for BCR::ABL1 p210 with high analytical sensitivity and precision. The assay was optimized and validated following CLSI guidelines. In-house plasmid standards were calibrated against internationally certified ERM-AD623 reference material. Analytical performance (specificity, sensitivity, precision, and linearity) and clinical validation were performed using 34 patient samples against the CE-IVD certified geneMAP BCR::ABL1 p210 IS-MMR kit. The assay demonstrated a low limit of detection (LoD) of 0.0030% BCR::ABL1/ABL1 ratio, corresponding approximately to an MR4.51-equivalent level, enabling reliable detection of low-level transcripts. No cross-reactivity with p190 variants was observed. Strong linearity was demonstrated across the MR1-equivalent to MR4.5-equivalent range. Precision met predefined acceptance criteria, with standard deviations below 0.28 MR units. Clinical validation demonstrated excellent correlation with the reference kit (Pearson's r = 0.979). This validated in-house assay demonstrates commercial-grade analytical performance, offering a cost-effective and accessible approach for reliable deep molecular response (DMR) assessment in local and research-oriented CML monitoring, particularly in resource-limited settings. - Source: PubMed
Publication date: 2026/07/15
Damerchiloo FatemehKaramali FatemehAmini AliShanaki MehrnooshBarati MahmoodSafa Majid - No large, randomized trials have compared three or more tyrosine kinase inhibitors (TKIs) in a single chronic myeloid leukemia (CML) cohort. Most studies are two-arm comparisons versus imatinib, or rely on indirect methods. - Source: PubMed
Mustafa Ali Moaath KZabor Emily CAbdurakhmanov KamillaZureigat HadilMohamed Ahmed NAlchirazi Muaz AlsabbaghDhakal AasthaMushtaq AliRehman NaveenBawwab AmeedBerube BryanKhatib LanaJain Akriti GMolina John CBalderman SophiaSingh AbhayGerds Aaron TSobecks RonaldAdvani Anjali SCarraway Hetty EKalaycio MattMukherjee Sudipto