2. Membrane Transporter/Ion Channel PI3K/Akt/mTOR Apoptosis
  3. GLUT PI3K Akt Apoptosis Bcl-2 Family
  4. 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.

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FKL-137

FKL-137 Chemical Structure

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FKL-137 Related Antibodies

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GLUT1 GLUT2 GLUT3 GLUT4

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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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

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[1].

IC50 & Target[1]

GLUT1

 

Akt

 

PI3K

 

Bax

 

Bcl-2

 

In Vitro

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.

FKL-137 Related Antibodies

Cell Viability Assay[1]

Cell Line: human erythroleukemia HEL cells, human erythroleukemia K562 cells, human normal hepatic stellate LX-2 cells, human hepatoma HepG2 cells
Concentration: 0.001 μM; 0.01 μM; 0.1 μM; 1 μM; 10 μM
Incubation Time: 24 h, 48 h, 72 h
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.

Apoptosis Analysis[1]

Cell Line: human erythroleukemia HEL cells, human erythroleukemia K562 cells
Concentration: 0.1 μM; 0.2 μM; 0.4 μM
Incubation Time: 48 h
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.

Western Blot Analysis[1]

Cell Line: human erythroleukemia HEL cells, human erythroleukemia K562 cells
Concentration: 0.1 μM; 0.2 μM; 0.4 μM
Incubation Time: 48 h
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.

Cell Viability Assay[1]

Cell Line: GLUT1-knockdown (shGLUT1) human erythroleukemia K562 cells
Concentration: 0.001 μM; 0.01 μM; 0.1 μM; 1 μM; 10 μM
Incubation Time: 48 h, 72 h
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.

Western Blot Analysis[1]

Cell Line: GLUT1-knockdown (shGLUT1) human erythroleukemia K562 cells
Concentration: 0.1 μM; 0.2 μM; 0.4 μM
Incubation Time: 48 h
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.
In Vivo

FKL-137 (1-10 mg/kg; i.p.; every 48 hours; 7 total doses) dose-dependently increases hematocrit, reduces splenomegaly and organ ratios, improves histopathological lesions, lowers spleen glucose and lactate levels, and downregulates metabolic proteins in Fr-MuLV-induced erythroleukemia mice, with the 10 mg/kg dose producing the most significant effects (p<0.001 vs. model group for hematocrit, spleen weight, and glucose content)[1].

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

Animal Model: BALB/c (8-10 week old male and female; Fr-MuLV-induced erythroleukemia model established at 6 weeks of age)[1]
Dosage: 1 mg/kg; 5 mg/kg; 10 mg/kg
Administration: i.p.; every 48 hours; 7 total doses
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.
Molecular Weight

392.37

Formula

C20H19F3N2O3
SMILES

CN(C1=CC=C(OC)C(OC)=C1)C2=CC(C(F)(F)F)=NC3=CC=CC(OC)=C32
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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FKL-137 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

FKL-137FKL137FKL 137GLUTPI3KAktApoptosisBcl-2 FamilyGlucose transporter Phosphoinositide 3-kinasePKBProtein kinase BLX-2 liver cellsK562 erythroleukemia cellsHEL erythroleukemia cellsPI3K/AKT signaling pathwayerythroleukemiaglucose metabolism-related proteinsapoptosisFriend virusHepG2 hepatoma cellsGLUT1Inhibitorinhibitorinhibit

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