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Gilteritinib (ASP2215)

Name: Gilteritinib (ASP2215)
Brand: Selleck Chemicals
SKU: S7754
Rating: 5 (22 reviews)

Catalog No.S7754

For research use only.

Gilteritinib (ASP2215) is a small-molecule FLT3/AXL inhibitor with IC50 values of 0.29 nM and 0.73 nM for FLT3 and AXL, respectively. It inhibits FLT3 at an IC50 value that was approximately 800-fold more potent than the concentration required to inhibit c-KIT (230 nM).

Gilteritinib (ASP2215) Chemical Structure

CAS No. 1254053-43-4

Selleck's Gilteritinib (ASP2215) has been cited by 22 publications

Purity & Quality Control

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FLT3 Signaling Pathway Map

Biological Activity

Description

Targets

FLT3 ^[1] (Cell-free assay)	Axl ^[1] (Cell-free assay)
0.29 nM	0.73 nM

In vitro

Gilteritinib demonstrates potent inhibitory activity against the internal tandem duplication (FLT3-ITD) and FLT3-D835Y point mutations in cellular assays using MV4-11 and MOLM-13 cells as well as Ba/F3 cells expressing mutated FLT3. Gilteritinib decreases the phosphorylation levels of FLT3 and its downstream targets in both cellular and animal models. Gilteritinib inhibits the activity of eight of the 78 tested kinases by over 50% at concentrations of either 1 nM (FLT3, LTK, ALK, and AXL) or 5 nM (TRKA, ROS, RET, and MER)^[1]. Gilteritinib treatment for 48h results in an induction of apoptosis in MV4-11 cells as determined by an increase in annexin V-positive cells. Gilteritinib also decreases the expression of anti-apoptotic proteins such as MCL-1, BCL2L10, and survivin, which are reported to be important in chemotherapy sensitivity, following 24h treatment^[2].

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Formulation	Activity Description	PMID

MV4-11 cells	NWDZZXF[S2WubDDjfYNt\SCjc4PhfS=>	MnjXNUwhOyxiMUCsJIFv\CB\|MDDuUS=>	MY[yOEBp	M3[yb3Rp\SCvZXHuJJBzd3CxcoTpc44hd2ZiTW[0MVEyKGOnbHzzJIlvKEdzIIDoZZNmKHencnWgd4lodmmoaXPhcpRtgSCrbnPy[YF{\WRiYYSg[4ltfGW{aYTpcoljKGOxbnPlcpRz[XSrb37zJI9nKDNiKE[5MlAmQyCSPECuNFEqKGGwZDCxNEBvVSBqN{CuO{U8KFB:MD6wNFEqNg>?	M13ydVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNzME[5NFE2Lz5\|MUC2PVAyPTxxYU6=
MOLM-13 cells	MXTBdI9xfG:\|aYOgZZN{[Xl?	NX\ZUJROOSxiMzygNVAtKDNyLDDhcoQhOTByIH7N	NH3wW3k1QCCq	MlS5d4lodmmoaXPhcpQhcW6lcnXhd4V{KGmwIITo[UBx\XKlZX70ZYdmKG:oIHHucoV5cW5iVj3wc5NqfGm4ZTDj[YxteyCjdDDjc45k\W62cnH0bY9veyCxZjCzNEBvVSBqM{KuNEUqKGGwZDCxNFAhdk1iKEWyMlQmMSC4ZYLzeZMh[2:wdILvcEApPC5zJTm=	MmHoQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzFyNkmwNVUoRjNzME[5NFE2RC:jPh?=
32D/TKD cells	MoP2SpVv[3Srb36gZZN{[Xl?	NVjo[VlGPTBibl5CpC=>	Mn\DOkBp	Mmr4TY5pcWKrdH;uJI9nKHSqZTDwbI9{eGixconsZZRqd25ib3[gRYt1KG:wIGSzNFg>	MUi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTVyN{[2NEc,Ojl3MEe2OlA9N2F-
TF-1 cells	NFzOTWNHfW6ldHnvckBie3OjeR?=	MV:wMEAzOCxiOECsJFIxOCCjbnSgOVAxKG6P	MVKxJIg>	NXnqW4FX\2mudHXybZRqdmmkIHjhd{BidiCLQ{WwJIFo[Wmwc4Sge4lt\C22eYDlJIMuU2m2IH;mJFExOiCwTR?=	Ml;lQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjd7MEi4PFEoRjJ5OUC4PFgyRC:jPh?=
BA/F3	MXnGeY5kfGmxbjDhd5NigQ>?			MXrJcohq[mm2aX;uJGF{e2G7OjDBJJJm[2:vYnnuZY51KHKndILveolzfXNid3HzJINz\WG2ZXSg[pJwdSCneIDy[ZN{cW:wIIDsZZNucWRiRlzBS{1GVUx2LVHMT5YyN3CPWD3pdoV{S0R6IHnuJJdpcWOqIHPEUmEh\m:{IFXNUGEuSUyNIH\1d4lwdiCycn;0[YlvKHZzIIfhd{BqdnSnZ4LheIVlNCCjbnSgbY5r\WO2ZXSgbY51dyCvb4Xz[UBtgW2yaH;p[EBk\WyuIHzpcoUhSkFxRkOgZ4VtdHNwIGXzbY5oKGFibXHncoV1cWNiYnXh[EBz\WGpZX70JIYtKEmFNUCgQUAxNjByMUWg{txONg>?	MXG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyzN\|AyPjJ{Lze+R4hGVUKOPD;hQi=>
BA/F3	M1zWUGZ2dmO2aX;uJIF{e2G7			NXPocmpvUW6qaXLpeIlwdiCDc4PhfVohSSC{ZXPvcYJqdmGwdDDy[ZRzd3[rcoXzJJdieyClcnXheIVlKG[{b32g[ZhxemW\|c3nvckBxdGG\|bXnkJGZNSUdvRV3MOE1CVEu4MT;wUXgucXKnc1PEPEBqdiC5aHnjbEBkTE6DIH\vdkBGVUyDLVHMT{BnfXOrb36gdJJwfGWrbjD2NUB4[XNiaX70[Ydz[XSnZDygZY5lKGmwanXjeIVlKGmwdH:gcY92e2VibIntdIhwcWRiY3XscEBtcW6nIFLBM2Y{KGOnbHzzMkBWe2mwZzDhJI1i\26ndHnjJIJm[WRicnXh[4VvfCCoLDDJR\|UxKD1iMD6wNFE2KM7:TT6=	M{jtSFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFM{ODF4MkKvK\|5EcEWPQly8M4E,
Vero	NGHiN41CdnSrdnnyZYwh[XO\|YYm=		MUWyOEBpeg>?	NIjkU5dCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBUSVKVLVPvWk0zKCi4aYLhcEB1cXSncjmgcYVie3W{ZXSgZpkheGyjcYXlJIF{e2G7IHnuJHZmem9iY3XscJMh[XRiTV;JJFAvODF{NTDh[pRmeiB{NDDodkwhUUN3MDC9JFYvPzZizszNMi=>	Mly4QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMN\|MxOTZ{Mj:nQmNpTU2ETEyvZV4>
Vero	NY\USIFPS2WubDD2bYFjcWyrdImgZZN{[Xl?		NEfaZmg4OiCqch?=	M4e0R2NmdGxidnnhZoltcXS7IH3lZZN2emWmIHL5JGNmdGyWaYTldk1IdG9iYYPzZZkhcW5iVnXyc{Bk\WyuczDheEBOV0liMD6wOUBi\nSncjC3NohzNCCFQ{WwJF0hOzdwMU[g{txONg>?	NID0PFU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmw{OzBzNkKyM{c,S2iHTVLMQE9iRg>?

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Assay

Methods	Test Index	PMID

Western blot

p-STAT5 / STAT5 / p-AKT / AKT / p-ERK / ERK ; p-c-kit / c-kit ; p-FLT3(Y591) / FLT3

28516360 27908881 30344940

In vivo

In vivo, gilteritinib is distributed at high levels in xenografted tumors after oral administration. The decreased FLT3 activity and high intratumor distribution of gilteritinib translates to tumor regression and improved survival in xenograft and intra-bone marrow transplantation models of FLT3-driven AML. This antitumor activity is associated with a durable inhibition of phospho-FLT3 and phospho-STAT5. Furthermore, treatment with gilteritinib decreases the leukemic burden and prolongs survival in a mouse IBMT model. No overt toxicity is seen in mouse models treated with gilteritinib^[1].

Protocol (from reference)

Cell Research: ^[1]	Cell lines: MV4-11 cells Concentrations: 0.1 nM, 1 nM, and 10 nM Incubation Time: 2 h Method: MV4-11 cells are treated with DMSO or increasing concentrations of gilteritinib for 2 hours. Immunoprecipitation and immunoblot for phosphorylated FLT3 and total FLT3 are performed.
Animal Research: ^[1]	Animal Models: MV4-11 xenografted mice (Nude mice) Dosages: 1 mg/kg, 6 mg/kg, and 10 mg/kg Administration: oral

References

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight	552.71
Formula	C₂₉H₄₄N₈O₃
CAS No.	1254053-43-4
Storage	3 years	-20°C	powder
Storage	2 years	-80°C	in solvent
Smiles	CCC1=C(N=C(C(=N1)C(=O)N)NC2=CC(=C(C=C2)N3CCC(CC3)N4CCN(CC4)C)OC)NC5CCOCC5

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Clinical Trial Information

NCT Number	Recruitment	Interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT04699877	Recruiting	Drug: Gilteritinib	Renal Impaired\|Gilteritinib\|Normal Renal Function\|Pharmacokinetics of ASP2215	Astellas Pharma Global Development Inc.\|Astellas Pharma Inc	January 28 2021	Phase 1
NCT04140487	Recruiting	Drug: Azacitidine\|Drug: Gilteritinib\|Drug: Venetoclax	Recurrent Acute Myeloid Leukemia\|Recurrent Chronic Myelomonocytic Leukemia\|Recurrent Myelodysplastic/Myeloproliferative Neoplasm\|Refractory Acute Myeloid Leukemia\|Refractory Chronic Myelomonocytic Leukemia\|Refractory Myelodysplastic/Myeloproliferative Neoplasm	M.D. Anderson Cancer Center	December 17 2019	Phase 1\|Phase 2
NCT03730012	Completed	Drug: gilteritinib\|Drug: atezolizumab	Acute Myeloid Leukemia (AML)\|Acute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) Mutation	Astellas Pharma Global Development Inc.\|Astellas Pharma Inc	June 19 2019	Phase 1\|Phase 2
NCT03964038	Completed	Drug: gilteritinib\|Drug: gilteritinib mini tablet	Healthy Volunteer	Astellas Pharma Global Development Inc.\|Astellas Pharma Inc	May 21 2019	Phase 1

(data from https://clinicaltrials.gov, updated on 2022-01-17)

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