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Cat. No.: HY-187532

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PFKL-IN-1

PFKL-IN-1 is an orally active PFKL inhibitor, with a human-derived IC₅₀ value of 52.63 nM and a K_d of 0.24 μM. PFKL-IN-1 directly binds to PFKL and inhibits its enzymatic activity. PFKL-IN-1 inhibits glycolysis, induces apoptosis and suppresses cell proliferation in breast cancer cells. PFKL-IN-1 exhibits antitumor efficacy in mouse models and enhances the therapeutic effect of anti-PD-L1 agents. PFKL-IN-1 can be used in breast cancer-related research.

Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.

Formule: C₃₉H₂₉BrCl₄F₆N₄S
Masse moléculaire:921.45

Stockage:

Please store the product under the recommended conditions in the Certificate of Analysis.

PFKL-IN-1 Chemical Structure

Stock

Quantité

Amount: USD 0.00

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Activité biologique
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
Help & FAQs
Classifications
Bioz

Activité biologique

Description

IC₅₀ & Target

^[1]

hPFKL

52.63 nM (IC₅₀)

hPFKL

0.24 μM (Kd)

Cellular Effect

Cell Line	Type	Value	Description	References
MCF7	IC50	1.05 μM	Antiproliferative activity against human MCF-7 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay. Antiproliferative activity against human MCF-7 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.	42487371
MDA-MB-231	IC50	1.24 μM	Antiproliferative activity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay. Antiproliferative activity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.	42487371
MDA-MB-468	IC50	0.85 μM	Antiproliferative activity against human MDA-MB-468 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay. Antiproliferative activity against human MDA-MB-468 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.	42487371
HCC1937	IC50	0.87 μM	Antiproliferative activity against human HCC1937 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay. Antiproliferative activity against human HCC1937 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay.	42487371

In Vitro

PFKL-IN-1 (Compound 10w) (1-100 μM; 1 h pre-incubation with lysate prior to Pronase treatment) binds directly to PFKL in lysates of MCF-7 and MDA-MB-468 breast cancer cells^[1].
PFKL-IN-1 (1-2 μM; 12-24 h) inhibits glycolysis in MCF-7 and MDA-MB-468 breast cancer cells in a PFKL-dependent manner, as evidenced by decreased levels of extracellular acidification rate (ECAR), glucose consumption and lactate production; this effect is completely abolished in PFKL-knockdown cells^[1].
PFKL-IN-1 (24 h) inhibits the enzymatic activity of PFKL and reduces FBP levels in MCF-7 and MDA-MB-468 breast cancer cells, and its antiproliferative effect is partially mediated by this inhibition^[1].
PFKL-IN-1 (48 h) potently inhibits the proliferation of MCF-7, MDA-MB-231, MDA-MB-468 and HCC1937 breast cancer cells, with IC₅₀ values ranging from 0.85 to 1.24 μM after 48 h of treatment^[1].
PFKL-IN-1 (1-4 μM; 48 h) inhibits DNA synthesis and proliferation of MCF-7 and MDA-MB-468 breast cancer cells^[1].
PFKL-IN-1 (initial treatment for 48 h, followed by 14-day incubation) inhibits the clonogenic capacity of MCF-7 and MDA-MB-468 breast cancer cells in a dose-dependent manner after 48 h of treatment^[1].
PFKL-IN-1 (0.25-1 μM; 48 h) inhibits the migration and invasion abilities of MCF-7 and MDA-MB-468 breast cancer cells in a dose-dependent manner^[1].
PFKL-IN-1 (48 h) induces G0/G1 cell cycle arrest in MCF-7 and MDA-MB-468 breast cancer cells, which correlates with decreased protein levels of cyclin D1 and CDK4^[1].
PFKL-IN-1 (1-4 μM; 48 h) induces apoptosis in MCF-7 and MDA-MB-468 breast cancer cells in a dose-dependent manner by upregulating the BAX/Bcl-2 ratio and activating caspase-3, and this effect depends on the expression of PFKL^[1].

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

Cell Proliferation Assay^[1]

Cell Line:

MCF-7 and MDA-MB-468 breast cancer cells
Concentration:

1, 2, 4 μM
Incubation Time:

48 h
Result:

Significantly reduced the number of EdU-positive cells in both MCF-7 and MDA-MB-468 cell lines, indicating inhibited DNA synthesis and cell proliferation.

Apoptosis Analysis^[1]

Cell Line:

MCF-7 and MDA-MB-468 breast cancer cells
Concentration:

1, 2, 4 μM
Incubation Time:

48 h
Result:

Increased apoptotic rates in a dose-dependent manner in both cell lines.
Upregulated the BAX/Bcl-2 ratio and cleaved caspase-3 protein levels in a dose-dependent manner.
Did not further modulate apoptosis-related protein levels in PFKL-knockdown cells.

Cell Migration Assay ^[1]

Cell Line:

MCF-7 and MDA-MB-468 breast cancer cells
Concentration:

0.25, 0.5, 1 μM
Incubation Time:

48 h
Result:

Significantly delayed wound closure in a dose-dependent manner in both cell lines, indicating reduced cell migratory capacity.

Cell Invasion Assay^[1]

Cell Line:

MCF-7 and MDA-MB-468 breast cancer cells
Concentration:

0.25, 0.5, 1 μM
Incubation Time:

48 h
Result:

Reduced the number of invaded cells in a dose-dependent manner in both cell lines, indicating reduced invasive capacity.

Parmacokinetics

Species	Dose	Route	T_max	T_1/2	C_max	AUC_0-t	AUC_0-∞	V_z	CL	MRT_0-∞	Bioavailability
Mice^[1]	1 mg/kg	i.v.	0.083 h	7.424 h	8767.998 ng/mL	5236.117 ng·h/mL	5496.937 ng·h/mL	1943.597 mL/kg	182.652 mL/h/kg	2.641 h	/
Mice^[1]	10 mg/kg	p.o.	2.500 h	4.963 h	182.809 ng/mL	1478.485 ng·h/mL	1203.429 ng·h/mL	/	/	5.507 h	2.8 %

In Vivo

PFKL-IN-1 (25-50 mg/kg; p.o.; once daily; for 12-14 consecutive days) inhibits breast cancer growth in a dose-dependent manner in the 4T1 syngeneic mouse model, modulates the tumor immune microenvironment, and enhances the anti-tumor efficacy of anti-PD-L1 immunotherapy^[1].

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

Animal Model:

BALB/c mice (equal number of male and female)^[1]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Achieved a tumor growth inhibition (TGI) rate of 21.4% at 25 mg/kg.
Achieved a tumor growth inhibition (TGI) rate of 59.5% at 50 mg/kg.
Caused no significant body weight loss in either treatment group.
Left serum levels of ALB, ALP, TG, CHO, and TP unchanged relative to controls.
Induced tumor necrosis in treated groups, with no pathological abnormalities detected in heart, liver, spleen, lung, or kidney.
Significantly reduced Ki67- and PCNA-positive proliferative cells in tumor tissues.

Animal Model:

BALB/c mice^[1]
Dosage:

50 mg/kg
Administration:

p.o.; daily; 12 days
Result:

Enhanced the infiltration of CD8+ T lymphocytes and M1-polarized macrophages, while reducing M2-type macrophages in the tumor microenvironment when used alone.
Achieved a tumor growth inhibition (TGI) rate of 72.5% when combined with anti-PD-L1 antibody, compared to 40.5% with anti-PD-L1 monotherapy.
Caused no significant body weight changes during treatment.

Chemical Information

Masse moléculaire 921.45
Formule C₃₉H₂₉BrCl₄F₆N₄S
SMILES

ClC1=C(CS/C(N[C@@H](CC2=CC=CC=C2)CN3C=[N+](C4=C3C=CC=C4)CC5=C(C=CC=C5Cl)Cl)=N\C6=CC(C(F)(F)F)=CC(C(F)(F)F)=C6)C(Cl)=CC=C1.[Br-]
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[1]. Wang M, et al. Targeting PFKL with S-Benzylisothiourea Imidazolium Salt Derivatives to Suppress Glycolysis and Treat Breast Cancer. Journal of medicinal chemistry. 2026 Jul 22.

Calculators

Calculateur de molarité

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Calculateur de dilution

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Bioz

Keywords

MOQ

Minimum order quantity

100 mg

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