(YourDigitalWall Editorial):- Dallas, Texas Nov 13, 2024 (Issuewire.com) – Arog Pharmaceuticals, Inc., a privately held late-stage biopharmaceutical company focused on the development of crenolanib and a related class of benzimidazole-based compounds for the treatment of leukemia and other diseases, today announced that long-term follow up data of crenolanib maintenance of crenolanib after allogeneic transplantation in FLT3 mutated acute myeloid leukemia (AML) will be presented at the 66th American Society of Hematology Annual Meeting and Exposition being held December 7-10, 2024, in San Diego, CA.
Poster Presentation Details, Abstract 1497
Authors: Betul Oran, MD, MS, David Marin, MD, Qaiser Bashir, MD, Sairah Ahmed, MD, Amanda L. Olson, MD, Uday Popat, MD, Partow Kebriaei, MD, Elizabeth J. Shpall, MD, Vinay Jain, MD, MBBS, and Richard E. Champlin, MD
Session Name: 616. Acute Myeloid Leukemias: Investigational Drug and Cellular Therapies
Session Date and Time: Saturday, December 7, 2024, 5:30 p.m. – 7:30 p.m. PT
Location: San Diego Convention Center, Halls G-H
Abstract Summary: Crenolanib, a type I, pan-FLT3 inhibitor, was administered on a daily basis to 30 patients with FLT3+ AML following allo-HSCT as maintenance therapy. Most patients (22) received crenolanib in CR1, with the balance receiving crenolanib following CR2, CR3, or with residual disease prior to transplant. Median follow-up time was 58.3 months and the 5-year RFS for the 19 patients in CR1 with FLT3-ITD treated was 78.9% and the 5-year OS was 84.2%. No increases in myelosuppression or GVHD were observed, and no cardiac (e.g., QT prolongation) or neurological (e.g., PRES) side effects occurred.
About Arog Pharmaceuticals, Inc.
Arog Pharmaceuticals is a US-based, late-stage biopharmaceutical company dedicated to developing its lead investigational drug candidate, crenolanib, and a related class of benzimidazole-based compounds to become best-in-class therapies in cancer indications with high unmet medical needs.
Arog was founded in 2010 to secure exclusive global rights to its product candidates from Pfizer. Since then, Arog has enrolled over 700 patients in completed or ongoing clinical trials in AML and advanced solid tumors.
About Crenolanib
Crenolanib is a next-generation type I TKI that selectively and potently inhibits signaling of wild-type and mutant isoforms of class III receptor tyrosine kinases FLT3 and PDGFR/.
About FLT3 AML
FLT3 mutated AML is an aggressive and deadly disease with limited targeted therapy options. FLT3 mutations are the most common driver mutations in AML, occurring in 25 – 33% of patients and are associated with increased rates of relapse and decreased survival. FLT3 mutations lead to constitutive activation of the tyrosine kinase function, making FLT3 inhibition an attractive drug target in AML patients. In addition, AML is a polyclonal disease, and multiple FLT3 mutations have been identified, including internal tandem duplications (ITD), mutations in the tyrosine kinase domain (TKD), and variant mutations. FLT3 mutations are generally regarded as poor prognostic markers in AML. Despite the approval of earlier-generation FLT3 inhibitors, an area of remaining high unmet medical need is in the treatment of residual FLT3-mutated AML following HSCT.
Contact
Edward McDonald
Head, Corporate Development
(YourDigitalWall Editorial):- Dallas, Texas Nov 13, 2024 (Issuewire.com) – Arog Pharmaceuticals, Inc., a privately held late-stage biopharmaceutical company focused on the development of crenolanib and a related class of benzimidazole-based compounds for the treatment of leukemia and other diseases, today announced that long-term follow up data of crenolanib maintenance of crenolanib after allogeneic transplantation in FLT3 mutated acute myeloid leukemia (AML) will be presented at the 66th American Society of Hematology Annual Meeting and Exposition being held December 7-10, 2024, in San Diego, CA.
Poster Presentation Details, Abstract 1497
Authors: Betul Oran, MD, MS, David Marin, MD, Qaiser Bashir, MD, Sairah Ahmed, MD, Amanda L. Olson, MD, Uday Popat, MD, Partow Kebriaei, MD, Elizabeth J. Shpall, MD, Vinay Jain, MD, MBBS, and Richard E. Champlin, MD
Session Name: 616. Acute Myeloid Leukemias: Investigational Drug and Cellular Therapies
Session Date and Time: Saturday, December 7, 2024, 5:30 p.m. – 7:30 p.m. PT
Location: San Diego Convention Center, Halls G-H
Abstract Summary: Crenolanib, a type I, pan-FLT3 inhibitor, was administered on a daily basis to 30 patients with FLT3+ AML following allo-HSCT as maintenance therapy. Most patients (22) received crenolanib in CR1, with the balance receiving crenolanib following CR2, CR3, or with residual disease prior to transplant. Median follow-up time was 58.3 months and the 5-year RFS for the 19 patients in CR1 with FLT3-ITD treated was 78.9% and the 5-year OS was 84.2%. No increases in myelosuppression or GVHD were observed, and no cardiac (e.g., QT prolongation) or neurological (e.g., PRES) side effects occurred.
About Arog Pharmaceuticals, Inc.
Arog Pharmaceuticals is a US-based, late-stage biopharmaceutical company dedicated to developing its lead investigational drug candidate, crenolanib, and a related class of benzimidazole-based compounds to become best-in-class therapies in cancer indications with high unmet medical needs.
Arog was founded in 2010 to secure exclusive global rights to its product candidates from Pfizer. Since then, Arog has enrolled over 700 patients in completed or ongoing clinical trials in AML and advanced solid tumors.
About Crenolanib
Crenolanib is a next-generation type I TKI that selectively and potently inhibits signaling of wild-type and mutant isoforms of class III receptor tyrosine kinases FLT3 and PDGFR/.
About FLT3 AML
FLT3 mutated AML is an aggressive and deadly disease with limited targeted therapy options. FLT3 mutations are the most common driver mutations in AML, occurring in 25 – 33% of patients and are associated with increased rates of relapse and decreased survival. FLT3 mutations lead to constitutive activation of the tyrosine kinase function, making FLT3 inhibition an attractive drug target in AML patients. In addition, AML is a polyclonal disease, and multiple FLT3 mutations have been identified, including internal tandem duplications (ITD), mutations in the tyrosine kinase domain (TKD), and variant mutations. FLT3 mutations are generally regarded as poor prognostic markers in AML. Despite the approval of earlier-generation FLT3 inhibitors, an area of remaining high unmet medical need is in the treatment of residual FLT3-mutated AML following HSCT.
Contact
Edward McDonald
Head, Corporate Development
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