KF-1601
/ ImmunoForge
- LARVOL DELTA
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April 15, 2025
KF1601, a dual inhibitor of BCR::ABL1 and FLT3, overcomes drug resistance in FLT3+ blast phase chronic myeloid leukemia.
(PubMed, Mol Cancer)
- "Furthermore, KF1601 effectively inhibited the FLT3 signaling pathway in imatinib-resistant K562 cells expressing FLT3 and TAZ, suppressing cell proliferation through dual inhibition of BCR::ABL1 and FLT3. In summary, KF1601 demonstrated promising preclinical efficacy in overcoming resistance mechanisms, including the BCR::ABL1T315I mutation, while also addressing FLT3 signaling implicated in BP-CML progression. Unlike existing therapies such as ponatinib, KF1601 offers a favorable safety profile, potentially minimizing the risk of life-threatening adverse effects."
Journal • Cardiovascular • Chronic Myeloid Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Oncology • Thrombosis • ABL1 • FLT3 • TAFAZZIN
January 14, 2025
…KF1601, a chronic myeloid leukemia treatment, phase 1 clinical trial IND approved by MFDS
(PRNewswire)
- "...ImmunoForge also announced that it has received approval for the phase 1 clinical trial IND for 'KF1601 (development code name)', a treatment for Chronic Myelogenous Leukemia (CML), from the Korea Ministry of Food and Drug Safety."
New P1 trial • Chronic Myeloid Leukemia
May 15, 2024
KF-1601, A DUAL INHIBITOR BCR::ABL1 AND FLT3 , OVERCOMES DRUG RESISTANCE IN FLT3+ BLAST PHASE CHRONIC MYELOGENOUS LEUKEMIA
(EHA 2024)
- "To evaluate KF1601's efficacy inovercoming drug-resistance associated with FLT3, we utilized imatinib-resistant K562 cells with FLT3overexpression, and drug-resistant CML cells obtained from BP CML patients. BP CML poses significant clinical challenges due to its drug resistance, resulting from BCR::ABL1-dependentmutations and BCR::ABL1-independent pathways. KF1601, a dual inhibitor targeting both BCR::ABL1 and FLT3,demonstrates promising preclinical efficacy in overcoming resistance mechanisms, including theBCR::ABL1T315I mutation, while also addressing FLT3-mediated signaling implicated in BP CML progression. Unlike existing therapies such as ponatinib, KF1601 offers a favorable safety profile, potentially minimizing therisk of life-threatening adverse effects."
Cardiovascular • Chronic Myeloid Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Oncology • Thrombosis • ABL1 • FLT3 • KDR • TAFAZZIN
December 03, 2023
KF1601, a Novel Orally Bioavailable Inhibitor of BCR-ABL1 T315I without Inducing Thrombotic Microangiopathy
(ASH 2023)
- "3) In murine models using Ba/F3 Bcr-Abl T315I cell line, it showed promising in vivo antitumor efficacy, comparable to that of ponatinib; 4) In animal models, it did not cause thrombotic microangiopathy, a major mechanism of ponatinib's toxicity. In summary, KF1601 is a promising drug candidate for safely treating CML patients with drug-resistant Bcr-Abl T315I mutation."
Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology • ABL1 • BCR
March 31, 2023
KF1601; a novel orally bioavailable inhibitor of Bcr-Abl T315I; without thrombotic microangiopathy
(ICKSH 2023)
- "1) It inhibited kinase functions of both Bcr-AblWT and Bcr-AblT315I with nanomolar IC50 values; 2) In orthotopic in vivo models using Ba/F3 Bcr-AblT315I cell line, it showed promising in vivo antitumor efficacy, comparable to that of ponatinib; 3) In animal models, it did not cause thrombotic microangiopathy, a major mechanism of ponatinib’s toxicity. In summary, KF1601 is a promising drug candidate for safely treating CML patients with drug-resistant Bcr-AblT315I mutation"
Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology • ABL1 • BCR
March 11, 2021
[VIRTUAL] KF1601, a novel orally bioavailable inhibitor of Bcr-Abl T315I, without inducing thrombotic microangiopathy
(AACR 2021)
- "Herein, we report KF1601, a novel orally bioavailable TKI: 1) KF1601 inhibited kinase functions of both Bcr-AblWT and Bcr-AblT315I with nanomolar IC50 values; 2) In xenograft models using Ba/F3 Bcr-AblT315I cell line, it showed promising in vivo antitumor efficacy, comparable to that of ponatinib; 3) In animal models, it did not cause thrombotic microangiopathy, a major mechanism of ponatinib’s toxicity. In summary, KF1601 is a promising drug candidate for safely treating CML patients with drug-resistant Bcr-AblT315I mutation."
Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology
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