FKL-137
FKL-137 is a GLUT1 and PI3K/AKT signaling pathway inhibitor. FKL-137 binds to GLUT1, reduces glucose uptake and lactate secretion, downregulates glucose metabolism-related proteins, and inhibits erythroleukemia cell proliferation. FKL-137 downregulates PI3K, p-PI3K, AKT, p-AKT levels, disrupts the PI3K/AKT-GLUT1 positive feedback loop, and suppresses erythroleukemia cell proliferation. FKL-137 induces apoptosis via upregulated Bax, Cleaved-PARP and downregulated Bcl-2, PARP. FKL-137 can be used for the research of erythroleukemia.
For research use only. We do not sell to patients.
- Formula: C20H19F3N2O3
- Molecular Weight:392.37
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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- References
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Help & FAQs
Biological Activity
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GLUT1 |
Akt |
PI3K |
Bax |
Bcl-2 |
FKL-137 (0.001-10 μM; 24-72 h) potently inhibits the proliferation of HEL and K562 erythroleukemia cells, while exhibiting relative safety in normal LX-2 liver cells compared to HepG2 hepatoma cells[1].
FKL-137 (0.1-0.4 μM; 48 h) induces apoptotic nuclear changes in HEL and K562 erythroleukemia cells[1].
FKL-137 (0.1-0.4 μM; 48 h) induces dose-dependent apoptosis in HEL and K562 erythroleukemia cells, with significant apoptotic populations detected at all tested concentrations in K562 cells and at 0.2-0.4 μM in HEL cells[1].
FKL-137 (0.1-0.4 μM; 48 h) modulates apoptosis-related protein expression in HEL and K562 erythroleukemia cells by upregulating Bax and Cleaved-PARP and downregulating Bcl-2 and PARP[1].
FKL-137 (0.1-0.4 μM; 48 h) downregulates the expression of glucose metabolism-related proteins HK2, PKM2, and LDH in HEL and K562 erythroleukemia cells[1].
FKL-137 (0.1-0.4 μM; 48 h) dose-dependently downregulates the protein levels of PI3K, p-PI3K, AKT, and p-AKT in HEL and K562 erythroleukemia cells[1].
FKL-137 (0.1-0.4 μM; 6-24 h) inhibits glucose uptake and lactate secretion in HEL and K562 erythroleukemia cells in a dose- and time-dependent manner, with significant effects observed as early as 6 h[1].
FKL-137 (0.001-10 μM; 2 h) increases the thermal stability of GLUT1 in K562 erythroleukemia cells without altering total GLUT1 protein levels at 0.01-1 μM[1].
FKL-137 (0-0.6 μM; 6 h) inhibits GLUT1-mediated glucose uptake in K562 erythroleukemia cells with an IC50 of 0.15 μM, and its inhibitory effect is reduced in high-glucose media, confirming competitive targeting of GLUT1[1].
FKL-137 (0.1-0.4 μM) reduces GLUT1 expression in HEL erythroleukemia cells in vitro in a dose-dependent manner[1].
FKL-137 (0.001-10 μM; 48-72 h) exhibits significantly stronger dose- and time-dependent anti-proliferative effects on GLUT1-knockdown K562 erythroleukemia cells at 72 h compared to negative control cells[1].
FKL-137 (0.1-0.4 μM; 6-24 h) further inhibits glucose uptake and lactate secretion in GLUT1-knockdown K562 erythroleukemia cells, with significant effects detected within 12 h[1].
FKL-137 (0.1-0.4 μM; 48 h) modulates the expression of compensatory upregulated glucose metabolism-related proteins HK2 and LDH in GLUT1-knockdown K562 erythroleukemia cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human erythroleukemia HEL cells, human erythroleukemia K562 cells, human normal hepatic stellate LX-2 cells, human hepatoma HepG2 cells
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Concentration:0.001 μM; 0.01 μM; 0.1 μM; 1 μM; 10 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Exerted significant, time- and dose-dependent inhibitory effects on HEL and K562 cell proliferation.
Achieved IC50 values of 0.6 μmol/L (24 h), 0.25 μmol/L (48 h), and 0.1 μmol/L (72 h) in HEL cells.
Achieved IC50 values of 0.8 μmol/L (24 h), 0.4 μmol/L (48 h), and 0.2 μmol/L (72 h) in K562 cells.
Exhibited hepatotoxicity safety index values of 1.65 (24 h), 1.66 (48 h), and 2.29 (72 h), indicating relative safety.
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Cell Line:human erythroleukemia HEL cells, human erythroleukemia K562 cells
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Concentration:0.1 μM; 0.2 μM; 0.4 μM
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Incubation Time:48 h
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Result:Induced characteristic apoptotic morphological changes including nuclear condensation, fragmentation, and chromatin margination in both HEL and K562 cells.
Showed effects increasing with compound concentration.\nCaused a dose-dependent increase in apoptotic cell populations in both cell lines.
Increased early and late apoptosis rates significantly at 0.2 μM and 0.4 μM in HEL cells.
Increased early and late apoptosis rates significantly at all tested concentrations, with the highest effects at 0.4 μM in K562 cells.
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Cell Line:human erythroleukemia HEL cells, human erythroleukemia K562 cells
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Concentration:0.1 μM; 0.2 μM; 0.4 μM
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Incubation Time:48 h
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Result:Dose-dependently upregulated pro-apoptotic Bax and Cleaved-PARP protein expression in both HEL and K562 cells compared to DMSO controls.
Downregulated anti-apoptotic Bcl-2 and full-length PARP protein expression in both HEL and K562 cells compared to DMSO controls.\nDose-dependently downregulated the expression of glucose metabolism-related proteins HK2, PKM2, and LDH in both HEL and K562 cells compared to DMSO controls.\nDose-dependently downregulated the protein levels of PI3K, p-PI3K, AKT, and p-AKT in HEL and K562 cells.
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Cell Line:GLUT1-knockdown (shGLUT1) human erythroleukemia K562 cells
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Concentration:0.001 μM; 0.01 μM; 0.1 μM; 1 μM; 10 μM
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Incubation Time:48 h, 72 h
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Result:Exerted dose- and time-dependent anti-proliferative effects on GLUT1-knockdown K562 cells.
Showed significantly stronger inhibitory activity at 72 h compared to negative control (NC) cells.
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Cell Line:GLUT1-knockdown (shGLUT1) human erythroleukemia K562 cells
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Concentration:0.1 μM; 0.2 μM; 0.4 μM
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Incubation Time:48 h
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Result:Modulated the expression of compensatory upregulated glycolytic enzymes HK2 and LDH in GLUT1-knockdown K562 cells, where GLUT1 knockdown caused compensatory upregulation of HK2 and LDH.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (8-10 week old male and female; Fr-MuLV-induced erythroleukemia model established at 6 weeks of age)[1]
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Dosage:1 mg/kg; 5 mg/kg; 10 mg/kg
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Administration:i.p.; every 48 hours; 7 total doses
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Result:Increased hematocrit to ~42% at 1 mg/kg, ~43% at 5 mg/kg, and ~55% at 10 mg/kg.
Reduced spleen weight to ~0.9 g at 1 mg/kg, ~0.4 g at 5 mg/kg, and ~0.2 g at 10 mg/kg.
Significantly reduced liver and spleen organ ratios across all doses; no significant changes to heart, lung, or kidney organ ratios were observed.
Significantly reduced pathological mitosis and tumor cell infiltration foci in spleen tissue across all doses compared to the model group.
Significantly reduced white blood cell infiltration in liver tissue across all doses compared to the model group; no significant histopathological changes were observed in heart, lung, or kidney tissues.
Reduced spleen glucose content to ~0.22 mmol/g and lactate content to ~0.28 mmol/g at 1 mg/kg; reduced spleen glucose content to ~0.12 mmol/g and lactate content to ~0.3 mmol/g at 5 mg/kg; reduced spleen glucose content to ~0.08 mmol/g and lactate content to ~0.3 mmol/g at 10 mg/kg.
Downregulated the expression of HK2 and LDH proteins in spleen tissue across all doses compared to the model group.
Chemical Information
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Molecular Weight 392.37
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Formula C20H19F3N2O3
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SMILES
CN(C1=CC=C(OC)C(OC)=C1)C2=CC(C(F)(F)F)=NC3=CC=CC(OC)=C32
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
FKL-137 Related Classifications
HY-183069 Related Classifications
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