2. Protein Tyrosine Kinase/RTK Stem Cell/Wnt JAK/STAT Signaling PI3K/Akt/mTOR MAPK/ERK Pathway Apoptosis Cell Cycle/DNA Damage Epigenetics
  3. FLT3 STAT Akt ERK Caspase PARP Bcl-2 Family Apoptosis
  4. FLC-8

FLC-8 is an orally active FLT3 inhibitor with IC50 values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia.

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FLC-8

FLC-8 Chemical Structure

CAS No. : 3100242-36-9

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FLC-8 Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

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Description

FLC-8 is an orally active FLT3 inhibitor with IC50 values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia[1].

IC50 & Target[1]

STAT5

 

ERK

 

Akt

 

Caspase 3

 

PARP

 

Bcl-2

 

Bax

 

bad

 

In Vitro

FLC-8 (3.5 h) potently inhibits FLT3-WT kinase activity with an IC50 of 10.2 nM[1].
FLC-8 (50 μM; 24 h) covalently binds to FLT3 kinase domain at the Cys807 residue[1].
FLC-8 (72 h) potently inhibits MV4-11 and MOLM-13 cell proliferation with IC50 values of 0.28 nM and 2.45 nM, respectively[1].
FLC-8 (72 h) potently inhibits proliferation of BaF3-FLT3ITD, BaF3-FLT3ITD-G697R, and BaF3-FLT3ITD-N676D cells with IC50 values of 3.10 nM, 11.6 nM, and 24.10 nM respectively, while showing reduced activity against other FLT3 mutant BaF3 cell lines[1].
FLC-8 (1 μM) demonstrates a narrow kinome inhibition spectrum with an S10 score of 0.096, potently inhibiting FLT3-WT, FLT3-ITD, PDGFRα, NCOA4-RET, and RET L730I at 1 μM[1].
FLC-8 (0.1-100 nM; 24 h) induces dose-dependent G0-G1 phase arrest in MV4-11 and MOLM-13 AML cells after 24 h incubation[1].
FLC-8 (0.1-100 nM; 24-72 h) induces dose-dependent apoptosis in MV4-11 and MOLM-13 AML cells over 24, 48, and 72 h[1].
FLC-8 (0.1-30 nM) induces apoptosis in MV4-11 cells via activation of the intrinsic apoptotic pathway, as shown by upregulation of pro-apoptotic genes/proteins, downregulation of anti-apoptotic BCL-2, cleavage of caspase-3 and PARP, and DNA fragmentation detected by TUNEL staining[1].
FLC-8 (0.1-30 nM; 12 h) inhibits FLT3 autophosphorylation and downstream STAT5, AKT, and ERK phosphorylation in a dose-dependent manner in MV4-11 cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

FLC-8 Related Antibodies

Cell Cycle Analysis[1]

Cell Line: MV4-11 and MOLM-13 AML cells
Concentration: 0.1, 1, 10, 100 nM
Incubation Time: 24 h
Result: Induced dose-dependent G0-G1 phase arrest in both cell lines.
Increased the G0-G1 population in MOLM-13 cells to 86.4% (from 52.0% in control) at 100 nM.
Increased the G0-G1 population in MV4-11 cells to 48.9%, 57.5%, 80.1%, and 87.0% at 0.1, 1, 10, and 100 nM respectively.

Apoptosis Analysis[1]

Cell Line: MV4-11 and MOLM-13 AML cells
Concentration: 0.1, 1, 10, 100 nM
Incubation Time: 24, 48, 72 h
Result: Induced dose-dependent apoptosis in both cell lines.
In MOLM-13 cells, apoptosis rates were 7.91-21.60% (24 h), 3.89-45.52% (48 h), and 3.69-73.90% (72 h).
In MV4-11 cells, apoptosis rates were 7.69-19.11% (24 h), 13.33-46.9% (48 h), and 7.61-71.20% (72 h).
Exceeded 70% apoptosis rates in both cell lines at 100 nM and 72 h.

Western Blot Analysis[1]

Cell Line: MV4-11 AML cells
Concentration: 0.1, 0.3, 1.0, 3.0, 10, 30 nM
Incubation Time: 12 h
Result: Potently inhibited FLT3 autophosphorylation in a dose-dependent manner, with significant suppression at 10 nM.
Reduced phosphorylation levels of STAT5, AKT, and ERK in a concentration-dependent fashion.
Exhibited superior inhibition of FLT3-mediated signaling at 30 nM compared to Quizartinib (HY-13001).
Parmacokinetics
Species Dose Route T1/2 C0 AUC0-t AUC0-∞ MRT0-t MRT0-∞ CL Tmax Cmax F
Mice[1] 1 mg/kg i.v. 0.2 h 629.0 ng/mL 106.5 ng·h/mL 112.0 ng·h/mL 0.1 h 0.2 h 9.0 L/h/kg / / /
Mice[1] 10 mg/kg p.o. 0.6 h / 109.9 ng·h/mL 125.4 ng·h/mL 0.7 h 0.9 h / 0.3 h 120.4 ng/mL 10.3 %
In Vivo

FLC-8 (10-50 mg/kg; i.p.; daily; 14 days) delivers potent, dose-dependent antitumor activity against MV4-11 AML xenografts, achieving a maximum tumor growth inhibition of 178% at 50 mg/kg with a favorable safety profile[1].
FLC-8 (10-50 mg/kg; p.o., i.p.; daily; 14 days) exhibits modest, dose-dependent antitumor activity against BaF3-FLT3-ITD-G697R AML xenografts, with the highest efficacy (TGI = 32%) achieved at an oral dose of 50 mg/kg[1].
FLC-8 (1-10 μM; immersion; 24 hours) demonstrates a favorable hematopoietic safety profile in transgenic zebrafish, with no significant impairment of neutrophil production at concentrations up to 10 μM[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: NOD/SCID (female, 4-5 weeks old, 18-20 g, subcutaneous inoculation of MV4-11 FLT3-ITD-expressing cells)[1]
Dosage: 10 mg/kg; 25 mg/kg; 50 mg/kg
Administration: i.p.; daily; 14 days
Result: Elicited dose-dependent tumor growth inhibition with TGI values of 136%, 163%, and 178% at 10, 25, and 50 mg/kg, respectively.
Achieved inhibitory rates (IR) based on final tumor weight of 25.0%, 48.2%, and 78.6% at 10, 25, and 50 mg/kg, respectively.
Induced dose-dependent tumor cell necrosis, reduced Ki67 staining, increased TUNEL staining, and reduced phosphorylated STAT5 in tumor tissues.
Animal Model: Balb/c nude (female, 6-8 weeks old, 18-20 g, subcutaneous inoculation of BaF3-FLT3-ITD-G697R cells)[1]
Dosage: 10 mg/kg (p.o.); 50 mg/kg (p.o.); 10 mg/kg (i.p.)
Administration: p.o. (daily; 14 days); i.p. (daily; 14 days)
Result: Produced minimal tumor growth inhibition (TGI = 2%) with a tumor weight inhibitory rate of 13.4% at oral 10 mg/kg.
Improved efficacy to a TGI of 32% with a tumor weight inhibitory rate of 30.7% at oral 50 mg/kg.
Resulted in a TGI of 11% with a tumor weight inhibitory rate of 8.5% at intraperitoneal 10 mg/kg.
Animal Model: Eze-Rinka (3-4 months old)[1]
Dosage: 1 μM; 10 μM
Administration: immersion; 24 hours
Result: Did not significantly reduce neutrophil counts at either concentration when compared to the vehicle control group.
Molecular Weight

496.44

Formula

C24H19F3N6O3
CAS No.
SMILES

C=CC(NC1=C(C(F)(F)F)C=C(NC(NC2=CC=C(C3=C(C(N)=NO4)C4=NC(C)=C3)C=C2)=O)C=C1)=O
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Keywords:

FLC-83100242-36-9FLC8FLC 8FLT3STATAktERKCaspasePARPBcl-2 FamilyApoptosisCluster of differentiation antigen 135CD135Fms like tyrosine kinase 3PKBProtein kinase BExtracellular signal regulated kinasespoly ADP ribose polymerase AKTAML cellsSTAT5acute myeloid leukemiaMV4-11Cys807FLT3-N676DFLT3-G697RFLT3-WTInhibitorinhibitorinhibit

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