Gilteritinib - CAS 1254053-43-4
Catalog number: B0084-462531
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
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 invitro, among the 78 tyrosine kinases tested, ASP2215 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. ASP2215 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. ASP2215 decreased tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells. ASP2215 may have potential use in treating AML.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-462531 100 mg $499 In stock
B0084-462531 500 mg $1499 In stock
Bulk Inquiry
Solid powder
Gilteritinib; ASP2215; ASP-2215; ASP 2215.
Canonical SMILES:
Current Developer:
Astellas Pharma / Kotobuki Pharmaceutical Co., Ltd.
1.Combined effect of cabozantinib and gefitinib in crizotinib-resistant lung tumors harboring ROS1 fusions.
Kato Y;Ninomiya K;Ohashi K;Tomida S;Makimoto G;Watanabe H;Kudo K;Matsumoto S;Umemura S;Goto K;Ichihara E;Ninomiya T;Kubo T;Sato A;Hotta K;Tabata M;Toyooka S;Maeda Y;Kiura K Cancer Sci. 2018 Jul 27. doi: 10.1111/cas.13752. [Epub ahead of print]
The ROS1 tyrosine kinase inhibitor (TKI) crizotinib has shown dramatic effects in patients with non-small cell lung cancer (NSCLC) harboring ROS1 fusion genes. However, patients inevitably develop resistance to this agent. Therefore, a new treatment strategy is required for lung tumors with ROS1 fusion genes. Two lung cancer cell lines, HCC78 harboring SLC34A2-ROS1 and ABC-20 harboring CD74-ROS1, were used as cell line-based resistance models. Crizotinib-resistant HCC78R cells were established from HCC78. We comprehensively screened the resistant cells using a phosphor-receptor tyrosine kinase array and RNA sequence analysis by next-generation sequencing (NGS). HCC78R cells showed upregulation of HB-EGF and activation of EGFR phosphorylation and the EGFR signaling pathway. Recombinant HB-EGF or EGF rendered HCC78 cells or ABC-20 cells resistant to crizotinib. RNA sequence analysis by NGS revealed the upregulation of AXL in HCC78R cells. HCC78R cells showed marked sensitivity to EGFR-TKIs or anti-EGFR antibody treatment in vitro. Combinations of an AXL-inhibitor, cabozantinib or gilteritinib, and an EGFR-TKI were more effective against HCC78R cells than monotherapy with an EGFR-TKI or AXL inhibitor.
2.Clinical Profile of Gilteritinib in Japanese Patients with Relapsed/Refractory AML: an Open-Label Phase 1 Study.
Usuki K;Sakura T;Kobayashi Y;Miyamoto T;Iida H;Morita S;Bahceci E;Kaneko M;Kusano M;Yamada S;Takeshita S;Miyawaki S;Naoe T Cancer Sci. 2018 Jul 24. doi: 10.1111/cas.13749. [Epub ahead of print]
Gilteritinib, a novel, highly specific, potent fms-like tyrosine kinase 3/AXL inhibitor, demonstrated antileukemic activity in patients with relapsed/refractory acute myeloid leukemia. In this open-label, Phase 1 study (;NCT02181660;), Japanese patients (aged ≥18 years) with relapsed/refractory acute myeloid leukemia received once-daily gilteritinib escalating from 20 mg/day to 300 mg/day. Primary endpoints were safety/tolerability including the maximum tolerated dose and recommended dose; secondary endpoints were antileukemic activity and pharmacokinetics. Twenty-four Japanese patients with relapsed/refractory acute myeloid leukemia received once-daily oral gilteritinib in one of six dose-escalation cohorts (20, 40, 80, 120, 200, 300 mg/day). Gilteritinib was well tolerated. The maximum tolerated dose was 200 mg/day; dose-limiting toxicities were grade 3 tumor lysis syndrome (120 mg/day; n=1); and grade 3 elevated blood lactate dehydrogenase, amylase, blood creatine phosphokinase levels and syncope (all n=2; 300 mg/day). The recommended dose was 120 mg/day. The most common drug-related grade ≥3 adverse events were thrombocytopenia (n=4 [16.7%]) and increased blood creatine phosphokinase (n=3 [12.
3.Inhibition of FLT3 in AML: a focus on sorafenib.
Antar A;Otrock ZK;El-Cheikh J;Kharfan-Dabaja MA;Battipaglia G;Mahfouz R;Mohty M;Bazarbachi A Bone Marrow Transplant. 2017 Mar;52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24.
FMS-like tyrosine kinase 3 (FLT3) is one of the most commonly mutated genes in AML. FLT3 is mutated in ~30% of patients with AML, either by internal tandem duplications (FLT3-ITD) of the juxta-membrane domain or by a point mutation, usually involving the tyrosine kinase domain. Several FLT3 tyrosine kinase inhibitors are being evaluated in multiple studies aiming at improving outcomes. The most widely used is sorafenib, a potent multikinase inhibitor approved for hepatocellular carcinoma and renal cell carcinoma. Sorafenib monotherapy or in combination with conventional chemotherapy, has been evaluated in various settings in AML, including front-line, relapsed or refractory disease including post-allograft failures and, more recently, as post-transplant maintenance therapy. Encouraging data have emerged with several other agents like lestaurtinib, midostaurin, crenolanib, gilteritinib and quizartinib. Although transient responses to FLT3 inhibitors are often observed in case of disease relapse, the most promising approach is the use of FLT3 inhibitors either in combination with induction chemotherapy or as consolidation/maintenance therapy after allogeneic hematopoietic cell transplantation.
Molecular Weight Calculator Molarity Calculator Solution Dilution Calculator

Related FLT3 Products

CAS 630124-46-8 AST 487

AST 487
(CAS: 630124-46-8)

AST487 is a Ret kinase inhibitor/FLT3 inhibitor, which displays high selectivity and potency toward FLT3 as a molecular target, and which could potentially be u...

(CAS: 1370256-78-2)

FLT3-IN-1, a Flt3 inhibitor, has been found to have week activity against T lymphoma Jurkat cells and human lung cancer PC-9 and H292 cells. IC50: 10 nM (in vit...

CAS 301305-73-7 TCS-359

(CAS: 301305-73-7)

TCS-359 is a potent inhibitor of FLT3 with IC50 of 42 nM.

CAS 861214-33-7 5'-Fluoroindirubinoxime

(CAS: 861214-33-7)

5'-Fluoroindirubinoxime is an inhibitor of FMS-like receptor tyrosine kinase-3 (FLT3) (IC50 = 15 nM) with antiproliferative activity. It displays selectivity fo...

CAS 1132827-21-4 AC 220 dihydrochloride

AC 220 dihydrochloride
(CAS: 1132827-21-4)

AC 220 dihydrochloride is a potent and selective inhibitor of FMS-like tyrosine kinase-3 (FLT3) used for the treatment of AML.

CAS 1254053-43-4 Gilteritinib

(CAS: 1254053-43-4)

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 FLT...

UNC-2025 hydrochloride

UNC-2025 hydrochloride is the hydrochloride salt of UNC-2025, which is the Mer/FLT3 dual inhibitor.

CAS 387867-13-2 Tandutinib

(CAS: 387867-13-2)

Tandutinib, also known as MLN 518, is a piperazinyl quinazoline receptor tyrosine kinase inhibitor with antineoplastic activity. Tandutinib inhibits the autopho...

Chemical Structure

CAS 1254053-43-4 Gilteritinib

Quick Inquiry

Verification code

Featured Items