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Art. -Nr.: HY-184580

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KMG-732

KMG-732 is a dual-target drug targeting GAK and β-tubulin, with K_d values of 12.0 nM and 19.3 μM, respectively. KMG-732 exhibits broad-spectrum antiproliferative activity in various human cancer cell lines and directly binds to purified tubulin in vitro. KMG-732 reduces the phosphorylation level of AP2M1, induces G2/M phase cell cycle arrest, disrupts the microtubule network, and inhibits cancer cell migration and invasion. KMG-732 shows significant antitumor activity in organoid and in vivo xenograft models. KMG-732 can be used for cancer research.

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

Formel: C₂₃H₁₇N₇
Molecular Weight:391.43

Speicherung:

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

KMG-732 Chemical Structure

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Fluorescent Dye

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

Biologische Aktivität
- Beschreibung
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

Cellular Effect

Cell Line	Type	Value	References
MIA PaCa-2	GI50	2.97 nM	42298883
BXPC-3	GI50	16.46 nM	42298883
HCT-116	GI50	20.15 nM	42298883
DLD-1	GI50	16.62 nM	42298883
A549	GI50	8.54 nM	42298883
NCI-H522	GI50	9.37 nM	42298883
SK-HEP1	GI50	12.67 nM	42298883
HepG2	GI50	14.18 nM	42298883
MCF7	GI50	10.43 nM	42298883
MDA-MB-231	GI50	111.17 nM	42298883

In Vitro

KMG-732 (10 μM; 90 min) potently inhibits the polymerization of purified tubulin in vitro, with a V_max of 13.95 mO.D./min^[1].
KMG-732 (0.78-12.5 μM; 300 sec) exhibits binding affinity for purified tubulin in vitro, with a K_d value of 19.3 μM^[1].
KMG-732 (1000 nM; 1 h) binds selectively and potently to purified GAK kinase in vitro with a K_d of 12.0 nM, while exhibiting extremely weak binding affinity toward most other tested kinases^[1].
KMG-732 potently inhibits the activity of purified GAK kinase in vitro, with an IC₅₀ of 73 nM^[1].
KMG-732 (serial concentrations; 72 h) exhibits broad-spectrum antiproliferative activity against various human cancer cell lines in vitro: the GI50 values against pancreatic cancer Mia-paca2, KP2, and BxPC3 cells are 2.97, 10.84, and 16.46 nM, respectively; the GI50 values against colorectal cancer HCT116 and DLD-1 cells are 20.15 and 16.62 nM, respectively; the GI50 values against lung cancer A549 and H522 cells are 8.54 and 9.37 nM, respectively; the GI50 values against liver cancer SK-HEP-1 and HepG2 cells are 12.67 and 14.18 nM, respectively; the GI50 values against breast cancer MCF7 and MDA-MB-231 cells are 10.43 and 111.17 nM, respectively^[1].
KMG-732 (0.1 μM; 1-16 h) completely disrupts the microtubule network in HCT116 colorectal cancer cells, which is characterized by perinuclear aggregation of tubulin and disappearance of cytoplasmic filamentous structures; it also induces the translocation of α-tubulin to the depolymerized (soluble) fraction, confirming its microtubule-destabilizing activity^[1].
KMG-732 (1 μM; 6 h) reduces the levels of acetylated and detyrosinated α-tubulin (markers of stable microtubules) in HCT116 colorectal cancer cells within 6 hours of treatment^[1].
KMG-732 (0.1-10 μM; 4 h pre-incubation plus 2 h EBI treatment) competes with the colchicine-site probe EBI for binding to β-tubulin in HCT116 colorectal cancer cells^[1].
KMG-732 (10-100 nM) induces changes in the levels of mitotic regulatory proteins in HCT116 colorectal cancer cells (decreased Wee1 expression, increased Aurora A, Aurora B and Cyclin B1 expression), indicating the occurrence of mitotic arrest^[1].
KMG-732 (0.1 μM; 2-8 h) induces time-dependent G2/M phase arrest in HCT116, Mia-paca2 and BxPC3 cancer cells in vitro^[1].
KMG-732 (10 nM; 24 h) significantly inhibits migration and invasion of HCT116 colorectal cancer cells in vitro, reducing both migratory and invasive capacities by over 40%, and this effect occurs without a decrease in cell viability^[1].
KMG-732 (0.1-1000 nM; 2 weeks) potently inhibits long-term colony formation of HCT116 colorectal cancer cells in vitro, with complete inhibition achieved at concentrations ≥100 nM^[1].
KMG-732 (72 h) maintains potent antiproliferative activity in both parental K562 leukemia cells (GI₅₀ = 20.7 nM) and P-gp-overexpressing K562A leukemia cells (GI₅₀ = 14.8 nM).
KMG-732 (0.002-10 μM) exhibits anti-tumor activity in intestinal tumor organoids derived from Apc^(1638n/+) mice, with an IC50 of 0.021 μM[1].

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

Immunofluorescence^[1]

Cell Line:

HCT116 colorectal cancer cells
Concentration:

0.1 μM
Incubation Time:

1 h
Result:

Caused complete collapse of organized α- and β-tubulin filament networks, with tubulin aggregating in perinuclear regions.

Western Blot Analysis^[1]

Cell Line:

HCT116 colorectal cancer cells
Concentration:

1 μM
Incubation Time:

6 h
Result:

Caused a rapid and significant decrease in levels of acetylated and detyrosinated α-tubulin (markers of stable, polymerized microtubules), while total α-tubulin levels remained unchanged.

Cell Cycle Analysis^[1]

Cell Line:

HCT116, Mia-paca2, and BxPC3 cancer cells
Concentration:

0.1 μM
Incubation Time:

0, 2, 4, 6 and 8 h
Result:

KMG-732 induces rapid, time-dependent accumulation of cells in the G2/M phase across all cell lines tested, with HCT116 cells showing an absolute increase of approximately 25 percentage points in the G2/M population after 8 hours of treatment.

Cell Invasion Assay^[1]

Cell Line:

HCT116 colorectal cancer cells
Concentration:

10 nM
Incubation Time:

24 h
Result:

Significantly reduces both migration and invasion of HCT116 colorectal cancer cells in Transwell assays, with both capacities inhibited by more than 40%.

Cell Proliferation Assay^[1]

Cell Line:

Drug-resistant K562A (P-gp overexpressing) and parental K562 leukemia cells
Concentration:

Serial concentrations
Incubation Time:

72 h
Result:

Showed comparable antiproliferative activity in parental K562 cells (GI₅₀ = 20.7 nM) and P-gp-overexpressing K562A cells (GI₅₀ = 14.8 nM), whereas colchicine showed a ~85-fold increase in GI₅₀ in K562A cells relative to parental K562 cells.

Cell Migration Assay ^[1]

Cell Line:

HCT116 colorectal cancer cells
Concentration:

10 nM
Incubation Time:

24 h
Result:

Significantly suppresses the migratory capacity of HCT116 colorectal cancer cells in a wound-healing assay, without affecting cell viability.

Parmacokinetics

Species	Dose	Route	T_max	C_max	T_1/2	AUC_last	MRT_last	Bioavailability	CL	V_ss
Mice^[1]	5 mg/kg	i.v.	/	/	4.6 h	1.09 μg·h/mL	1.39 h	/	4.72 L/h/kg	7.91 L/kg
Mice^[1]	10 mg/kg	i.p.	0.08 h	2.89 μg/mL	6.54 h	1.71 μg·h/mL	0.73 h	78.6 %	/	/
Mice^[1]	10 mg/kg	p.o.	0.25 h	0.29 μg/mL	4.21 h	0.33 μg·h/mL	2.73 h	15.0 %	/	/

In Vivo

KMG-732 (0.5 mg/kg; i.p.; once every 2 days; for 16 consecutive days) reduces tumor volume by 67.5% in HCT116 xenograft mice without affecting body weight^[1].
No significant toxicity or mortality is observed in C57BL/6 mice treated with KMG-732 (5-20 mg/kg; i.p.; single administration)^[1].

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

Animal Model:

athymic BALB/c nu/nu (male, 6 weeks old)^[1]
Dosage:

0.5 mg/kg
Administration:

i.p.; every other day; 16 days
Result:

Reduced tumor volume by 67.5% compared to the vehicle-treated group.
Maintained stable body weight throughout the study, with no significant weight loss observed.

Animal Model:

C57BL/6 (female, 8 weeks old)^[1]
Dosage:

5 mg/kg; 10 mg/kg; 20 mg/kg
Administration:

i.p.; single dose
Result:

Maintained stable body weight with no significant weight loss observed over 7 days.
Detected no severe clinical symptoms (e.g., tremors, hypoactivity).
Maintained 100% survival, with survival curves overlapping the vehicle group.

Chemical Information

Molecular Weight 391.43
Formel C₂₃H₁₇N₇
SMILES

CN1C=C(C(C2=CC=CC=C2)=N1)C3=C(C(N)=NC(C4=NNC5=C4C=CC=C5)=C3)C#N
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

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

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Park S, et al. Discovery and Pharmacological Characterization of a Dual-Acting 2-Amino-3-Cyanopyridine Inhibitor Targeting Microtubule Polymerization and GAK. Journal of medicinal chemistry. 2026 Jul 09;69(13):15489-15509.

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

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.

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100 mg

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