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Art. -Nr.: HY-187687

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Anticancer agent 359

Anticancer agent 359 is a ferroptosis inducer. Anticancer agent 359 inhibits the proliferation, colony formation and migration of bladder cancer cells in a concentration-dependent manner. Anticancer agent 359 induces ferroptosis by downregulating SREBP1 to inhibit FASN transcription, reducing the expression of NRF2/SLC7A11/GPX4, decreasing GSH, promoting ROS accumulation and lipid peroxidation; this effect is reversible by Ferrostatin-1 (HY-100579). Anticancer agent 359 acts synergistically with Talazoparib (HY-16106). Anticancer agent 359 inhibits tumor growth in vivo without obvious hepatotoxicity or nephrotoxicity. Anticancer agent 359 can be used in the research of bladder cancer.

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CAS. Nr.: 2740603-37-4
Formel: C₁₃H₁₈F₃N₅O
Molecular Weight:317.31

Speicherung:

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

Anticancer agent 359 Chemical Structure

CAS. Nr.: 2740603-37-4

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Use of MCE Products

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

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- In Vitro
- In Vivo
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Biologische Aktivität

Beschreibung

Alle Glutathione Peroxidase Isoform-spezifische Produkte anzeigen :

GPX1
GPX4

In Vitro

Anticancer agent 359 (compound 4c) potently inhibits the viability of human bladder cancer T24 and RT4 cells in a concentration-dependent manner following 72 h of treatment^[1].
Anticancer agent 359 (3-9 μM; 6-8 days) inhibits colony formation of human bladder cancer T24 and RT4 cells in a concentration-dependent manner, and achieves nearly complete inhibition at high concentrations^[1].
Anticancer agent 359 (3-9 μM; 24-48 h) inhibits the migration of human bladder cancer T24 and RT4 cells in a concentration-dependent manner in wound healing assays^[1].
Anticancer agent 359 (3-9 μM; 24 h) inhibits Transwell migration of human bladder cancer T24 cells in a concentration-dependent manner^[1].
Anticancer agent 359 (3-9 μM; 24 h) downregulates the mRNA and protein expression of FASN, as well as the protein expression of SREBP1, in a concentration-dependent manner in human bladder cancer T24 and RT4 cells^[1].
Anticancer agent 359 (3-9 μM; 24 h) induces ferroptosis in human bladder cancer T24 and RT4 cells, which is characterized by decreased GSH levels, increased MDA levels and increased ROS levels, and these effects are reversed by the ferroptosis inhibitor Ferrostatin-1 (HY-100579)^[1].
The antiproliferative effect of anticancer agent 359 (3-9 μM; 72 h) on human bladder cancer T24 cells is significantly attenuated by pretreatment with the ferroptosis inhibitor Ferrostatin-1, confirming that ferroptosis represents its key mechanism of action^[1].
Anticancer agent 359 (3-9 μM; 24 h) downregulates the protein expression of ferroptosis-related regulators NRF2, SLC7A11 and GPX4 in a concentration-dependent manner in human bladder cancer T24 and RT4 cells; FASN silencing enhances this effect, while FASN agonists attenuate it^[1].
Anticancer agent 359 (3-9 μM) acts synergistically with Talazoparib (HY-16106) to inhibit the viability, colony formation and migration ability of human bladder cancer T24 and RT4 cells. This ferroptosis-dependent sensitization effect can be reversed by pre-treatment with Ferrostatin-1^[1].
Combination of anticancer agent 359 (3-9 μM; 24 h) with Talazoparib enhances ferroptosis in human bladder cancer T24 and RT4 cells. The combination therapy more significantly downregulates the expression of SREBP1, FASN, NRF2, SLC7A11 and GPX4, and also induces more pronounced GSH depletion, ROS accumulation and MDA production^[1].

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

Cell Migration Assay ^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

3, 6, 9 μM
Incubation Time:

12 and 24 h (T24); 24 and 48 h (RT4)
Result:

Reduced wound closure (migration) in both T24 and RT4 cells in a concentration-dependent manner.
Reduced migration to ~0.2 relative to control at 9 μM after 24 h in T24 cells.
Reduced migration to ~0.1 relative to control at 9 μM after 48 h in RT4 cells.

Cell Migration Assay ^[1]

Cell Line:

human bladder cancer T24 cells
Concentration:

3, 6, 9 μM
Incubation Time:

24 h
Result:

Reduced the number of migrated T24 cells in a concentration-dependent manner.
Reduced migration to ~0.2 relative to control at 9 μM.

Cell Viability Assay^[1]

Cell Line:

human bladder cancer T24 cells
Concentration:

3, 6, 9 μM (post Ferrostatin-1 pretreatment)
Incubation Time:

6 h (Ferrostatin-1 pretreatment) then 72 h (target reagent incubation)
Result:

Rescued T24 cell viability from the inhibitory effect of the target reagent when pretreated with Ferrostatin-1.

Western Blot Analysis^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

3, 6, 9 μM; 3, 6, 9 μM (plus FASN siRNA); 3, 6, 9 μM (plus T0901317)
Incubation Time:

24 h
Result:

Downregulated protein expression of NRF2, SLC7A11, and GPX4 in both T24 and RT4 cells in a concentration-dependent manner.
Enhanced the reagent-induced downregulation of these proteins when combined with FASN siRNA.
Attenuated the FASN agonist T0901317's upregulatory effect on these proteins when combined with the reagent.

Immunofluorescence^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

3, 6, 9 μM (this compound); 5 μM (Ferrostatin-1)
Incubation Time:

24 h
Result:

Significantly increased intracellular ROS levels.
Ferrostatin-1 can reverse the compound-induced increase in ROS levels.

Western Blot Analysis^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

6 μM (this compound); 4 μM (Talazoparib)
Incubation Time:

24 h
Result:

Compared with monotherapy, combination therapy significantly downregulated the protein expression of SREBP1 and FASN.

Immunofluorescence^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

6 μM (this compound); 4 μM (Talazoparib)
Incubation Time:

24 h
Result:

Compared with monotherapy, combination therapy resulted in more significant intracellular ROS accumulation.

Western Blot Analysis^[1]

Cell Line:

human bladder cancer T24 and RT4 cell lines
Concentration:

6 μM (this compound); 4 μM (Talazoparib)
Incubation Time:

24 h
Result:

Compared with monotherapy, combination therapy significantly downregulated the expression of ferroptosis-related proteins NRF2, SLC7A11, and GPX4.

In Vivo

Anticancer agent 359 (compound 4c) (6 mg/kg; i.p.; daily; 14 days) suppresses bladder tumor growth in a subcutaneous xenograft model, enhances the antitumor efficacy of talazoparib, and exhibits negligible hepatorenal toxicity at the tested dose^[1].

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

Animal Model:

BALB/c nude mice (female, 4-6 weeks old, subcutaneous xenograft model)^[1]
Dosage:

6 mg/kg
Administration:

i.p.; daily; 14 days
Result:

Suppressed bladder tumor growth.
Nearly completely halted tumor progression when combined with talazoparib, resulting in a significantly lower average tumor weight compared to either single-agent group.
Downregulated tumor tissue expression of FASN, NRF2, SLC7A11, and GPX4.
Caused no notable body weight loss.
Maintained serum AST, ALT, and creatinine levels within physiological reference ranges.
Showed no evident organ damage in liver and kidney histology.

Chemical Information

CAS. Nr. 2740603-37-4
Molecular Weight 317.31
Formel C₁₃H₁₈F₃N₅O
SMILES

N=C(NC(NCCCC)=N)NC1=CC=C(OC(F)(F)F)C=C1
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]. Yao J, et al. The novel biguanide derivative 4C synergizes with talazoparib by inducing ferroptosis via the SREBP1/FASN/SLC7A11/GPX4 axis in bladder cancer[J]. Cell Death Discovery, 2026.

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)}

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Anticancer agent 359

Alle Glutathione Peroxidase Isoform-spezifische Produkte anzeigen

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