BMS-911543 JAK2 inhibitor
- Known as:
- BMS-911543 JAK2 suppressor
- Catalog number:
- a-1175
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ActivBio Active Biochem
- Gene target:
- BMS-911543 JAK2 inhibitor
Related genes to: BMS-911543 JAK2 inhibitor
- Gene:
- JAK2 NIH gene
- Name:
- Janus kinase 2
- Previous symbol:
- -
- Synonyms:
- JTK10
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2019-04-23
Related products to: BMS-911543 JAK2 inhibitor
Related articles to: BMS-911543 JAK2 inhibitor
- Chronic kidney disease (CKD) is characterized by progressive tubulointerstitial inflammation and fibrosis, particularly affecting the proximal tubule. Both proximal tubular epithelial cells and interstitial fibroblasts contribute to CKD progression through cell-cycle arrest and phenotypic transitions. The aim of the present study was to address whether lactic acidosis contributes to these processes. - Source: PubMed
Schulz Marie-ChristinDubourg VirginieSchaude LeaSchröder NatalieJanßen EvaGörlich IsabelleRuhs StefanieKopf MichaelGekle Michael - ATP-site resistance mutations, exemplified by T315I in BCR::ABL1, limit the durability of kinase inhibitor therapy in hematological malignancies. Allosteric sites outside the catalytic cleft offer an alternative: ligands that bind regulatory pockets can stabilize inactive conformations and retain activity against mutations that defeat ATP-site drugs. Several reviews have addressed this principle across the kinome, but none has applied a hematology-focused druggability appraisal anchored in the BCR::ABL1/asciminib precedent. This review fills that gap with two contributions: mechanistic evidence that crizotinib engages BCR::ABL1 through a putative dual ATP-site/myristoyl-pocket mechanism, supported by indirect evidence and pending direct structural confirmation; and a hypothesis linking recurrent synonymous mutations in non-receptor tyrosine kinases to transiently structured regulatory regions, as a strategy for identifying latent allosteric sites Asciminib is the proof of concept. It binds the MBP of ABL1, locking the kinase in an autoinhibited-like state without competing for ATP. In the ASCEMBL trial, it achieved a major molecular response rate of 25.5% at 24 weeks versus 13.2% for bosutinib in heavily pretreated CML, with better tolerability-the first regulatory-site inhibitor approved for a hematological malignancy. The question is whether this can extends further. Dual-site strategies may raise the barrier to resistance, but the structural and biochemical validation remains incomplete for FLT3, JAK2, and BTK. Asciminib resistance is already real: A337V and P465S mutations reduce binding, and bypass signaling adds another layer. Each approved allosteric agent-asciminib, trametinib, and ivosidenib-required extensive structural and functional validation before reaching the clinic; structural prediction alone is not enough. - Source: PubMed
Publication date: 2026/09/06
Marx AilieCohen MaorRuthardt MartinMahajna Jamal - A 45-year-old active woman without previously known significant medical history presented with acute neurologic deficits (National Institutes of Health Stroke Scale (NIHSS) score 3) following a low-voltage electrical shock to her right arm three days earlier. Computed tomography angiography demonstrated a thrombus in the proximal right subclavian artery just distal to the origin of the right vertebral artery, while brain imaging revealed multifocal posterior circulation infarcts involving the left thalamus, left occipital lobe, and right cerebellar hemisphere. An extensive evaluation did not identify a cardiac source of embolism, intracardiac shunt, or convincing arterial dissection. Hypercoagulable testing identified heterozygous Factor V Leiden, and subsequent outpatient hematologic evaluation established a diagnosis of JAK2-mutated essential thrombocythemia (ET), revealing previously unrecognized prothrombotic risk factors. The patient was treated initially with intravenous unfractionated heparin and subsequently transitioned to rivaroxaban, with complete radiographic resolution of the subclavian thrombus and neurological recovery to NIHSS 0 and modified Rankin Scale (mRS) 0 at discharge. Following the diagnosis of ET, aspirin therapy was initiated, and she remained on rivaroxaban at the time of manuscript preparation. Although causality cannot be established, the temporal relationship and anatomic distribution raise the possibility that electrical injury acted as a vascular trigger in a patient with an underlying predisposition to thrombosis. This case emphasizes the importance of vascular imaging and evaluation for competing prothrombotic conditions when neurologic deficits develop following electrical injury. - Source: PubMed
Publication date: 2026/09/04
MacLennan Logan PAshurst JohnBalandin Andrei - Splenic abscess is a rare but life-threatening condition whose diagnosis is frequently delayed because of its nonspecific presentation. Development of a splenic abscess following splenic infarction secondary to splenic artery thrombosis is exceptional, particularly when revealing an underlying myeloproliferative neoplasm. An 85-year-old woman presented to the emergency department after three weeks of intermittent confusion without fever, abdominal pain, or gastrointestinal symptoms. While neurological investigations were unrevealing, thoracoabdominal computed tomography unexpectedly demonstrated a large splenic abscess associated with splenic artery thrombosis and bilateral pulmonary emboli. Laboratory tests showed marked systemic inflammation and severe thrombocytosis. Ultrasound-guided percutaneous drainage isolated , and treatment with intravenous antibiotics and therapeutic anticoagulation was initiated. The patient's course was complicated by septic shock requiring intensive care admission but ultimately evolved favorably with prolonged antimicrobial therapy and continuous percutaneous drainage, avoiding splenectomy. Additional investigations identified deep vein thrombosis and confirmed JAK2 V617F-positive essential thrombocythemia as the cause of a systemic prothrombotic state leading to multiple arterial and venous thrombotic events. This case illustrates how splenic abscess may present solely as delirium in older adults, without localizing abdominal symptoms. Emergency physicians should consider occult intra-abdominal infection in elderly patients presenting with unexplained delirium and inflammatory syndrome. When unusual arterial and venous thromboses coexist, an underlying myeloproliferative disorder should be actively investigated. In selected patients, image-guided percutaneous drainage combined with prolonged antibiotic therapy may provide an effective spleen-preserving alternative to splenectomy. - Source: PubMed
Publication date: 2026/08/05
El Haddad SarahBoulos PaulKadou JoeKalisz Simon - The classical myeloproliferative neoplasms (MPNs) are driven by somatic variants in (), () and () genes. The heterogeneity in mutational frequency of and triple-negative MPNs between regions indicates that epidemiological studies in sub-Saharan Africa are required. - Source: PubMed
Publication date: 2026/08/20
Dicks Marthinus JNell Erica-MariSwanepoel CarmenAbdullah IbtisamChapanduka Zivanai C