Incyte Corp.’s mention of would-be “backup molecules” could bode well for findings yet to roll out with Mas-related G protein-coupled receptor X2 antagonist INCB-000262 in chronic spontaneous urticaria. Meanwhile, though, the news is not good, as Incyte said in a terse press release that it will pause enrollment in the ongoing phase II study with the drug because of in vivo preclinical toxicology findings.
Incyte Corp. has identified tyrosine-protein kinase JAK2 (V617F mutant) inhibitors reported to be useful for the treatment of cancer, hypereosinophilic syndrome, systemic mastocytosis and essential thrombocythemia, among others.
The newest data show increased survival times for heavily pretreated patients receiving Briacell Therapeutics Corp.’s breast cancer treatment. The company’s phase II results produced positive overall survival data using the cell-based immunotherapy Bria-IMT to treat late-stage metastatic breast cancer.
Wall Street promptly started speculating about the product’s odds in the graft-vs.-host disease (GVHD) marketplace shortly after Syndax Pharmaceuticals Inc. and Incyte Corp. scored U.S. FDA approval – well ahead of the Aug. 29 PDUFA date – of Niktimvo (axatilimab), an anti-CSF-1R antibody for the treatment of chronic disease after failure of at least two prior lines of systemic therapy in adult and pediatric patients weighing at least 40 kg (88.2 lbs.).
Incyte Corp. has synthesized diacylglycerol kinase α (DGK-α) and/or diacylglycerol kinase ζ (DGK-ζ) inhibitors reported to be useful for the treatment of cancer.
Macrogenics Inc., agreeing with an independent data monitoring committee, has discontinued dosing patients in the troubled phase II Tamarack study of vobramitamab duocarmazine as a second-line treatment for metastatic castration-resistant prostate cancer.
Researchers from Incyte Corp. and collaborators presented the preclinical profile of INCB-160058, an ATP-competitive small-molecule inhibitor of the JAK2 V617F mutant sparing its wild-type (WT) form, designed for the treatment of JAC2 V617F mutation-positive myeloproliferative neoplasms with potential as a first-in-class JAK2 V617-inhibiting drug.
Among the acquired mutations in the calreticulin (CALR) gene, both 52 bp deletion (del52) and 5 bp insertion (ins5) are among the most frequent and are linked to two different types of myeloproliferative neoplasms (MPNs).
Myeloproliferative neoplasms (MPNs) can only be cured, to date, using allogeneic stem cell transplantation which, in turn, only works for up to 20% of patients. As calreticulin (CALR) frameshift mutations are the second most common cause of MPNs, targeting this endoplasmic reticulum resident protein is one of the strategies emerging at the forefront of hematological malignancies research.