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Restrict the search for
gilteritinib
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There is one exact (name or code) match for gilteritinib
Status:
US Approved Rx
(2018)
Source:
NDA211349
(2018)
Source URL:
First approved in 2018
Source:
NDA211349
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Gilteritinib, also known as ASP2215, is a potent FLT3/AXL inhibitor, which showed potent antileukemic activity against AML with either or both FLT3-ITD and FLT3-D835 mutations. In in vitro, among the 78 tyrosine kinases tested, Gilteritinib inhibited FLT3, LTK, ALK, and AXL kinases by over 50% at 1 nM with an IC50 value of 0.29 nM for FLT3, approximately 800-fold more potent than for c-KIT, the inhibition of which is linked to a potential risk of myelosuppression. Gilteritinib inhibited the growth of MV4-11 cells, which harbor FLT3-ITD, with an IC50 value of 0.92 nM, accompanied with inhibition of pFLT3, pAKT, pSTAT5, pERK, and pS6. Gilteritinib decreased tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells. In previous preclinical studies, gilteritinib has demonstrated superior antitumor effects when given in combination with AraC and either DNR or IDR compared with combination chemotherapy. In November 2018, the FDA approved gilteritinib for treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with a FLT3 mutation as detected by an FDA-approved test.
Status:
US Approved Rx
(2018)
Source:
NDA211349
(2018)
Source URL:
First approved in 2018
Source:
NDA211349
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Gilteritinib, also known as ASP2215, is a potent FLT3/AXL inhibitor, which showed potent antileukemic activity against AML with either or both FLT3-ITD and FLT3-D835 mutations. In in vitro, among the 78 tyrosine kinases tested, Gilteritinib inhibited FLT3, LTK, ALK, and AXL kinases by over 50% at 1 nM with an IC50 value of 0.29 nM for FLT3, approximately 800-fold more potent than for c-KIT, the inhibition of which is linked to a potential risk of myelosuppression. Gilteritinib inhibited the growth of MV4-11 cells, which harbor FLT3-ITD, with an IC50 value of 0.92 nM, accompanied with inhibition of pFLT3, pAKT, pSTAT5, pERK, and pS6. Gilteritinib decreased tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells. In previous preclinical studies, gilteritinib has demonstrated superior antitumor effects when given in combination with AraC and either DNR or IDR compared with combination chemotherapy. In November 2018, the FDA approved gilteritinib for treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with a FLT3 mutation as detected by an FDA-approved test.
Status:
Possibly Marketed Outside US
Source:
Octaplasma by Octapharma Pharmazeutika Produktionsges M B H [Canada]
Source URL:
First approved in 2013
Source:
BLA125416
Source URL:
Class:
MIXTURE
Status:
Investigational
Source:
NCT04456621: Not Applicable Interventional Completed Local Control Rate
(2019)
Source URL:
Class:
PROTEIN
