1. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis
  2. Reactive Oxygen Species (ROS) Apoptosis Bcl-2 Family Caspase SHMT Methylenetetrahydrofolate Dehydrogenase (MTHFD) Cytochrome P450
  3. Anticancer agent 310

Anticancer agent 310 is an antitumor agent. Anticancer agent 310 releases nitric oxide to induce mitochondrial ROS burst, triggers mitochondrial dysfunction and activates the Bax/Bcl-2-Cyt c-Caspase-9/Caspase-3 apoptotic pathway. Anticancer agent 310 also reduces the levels of SHMT2 and MTHFD2, decreases the ratios of NADPH/NADP+ and GSH/GSSG, thereby disrupting redox homeostasis and exacerbating intracellular ROS accumulation. Anticancer agent 310 can be used in research related to gastric cancer.

For research use only. We do not sell to patients.

Anticancer agent 310

Anticancer agent 310 Chemical Structure

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Description

Anticancer agent 310 is an antitumor agent. Anticancer agent 310 releases nitric oxide to induce mitochondrial ROS burst, triggers mitochondrial dysfunction and activates the Bax/Bcl-2-Cyt c-Caspase-9/Caspase-3 apoptotic pathway. Anticancer agent 310 also reduces the levels of SHMT2 and MTHFD2, decreases the ratios of NADPH/NADP+ and GSH/GSSG, thereby disrupting redox homeostasis and exacerbating intracellular ROS accumulation. Anticancer agent 310 can be used in research related to gastric cancer[1].

In Vitro

Anticancer agent 310 (compound A9) (0.016-10 μM; 72 h) potently inhibits the proliferation of various human and murine tumor cell lines in vitro[1].
Anticancer agent 310 (1.6-40 nM; 12-14 days) inhibits the long-term colony-forming ability of HGC27 and AGS gastric cancer cells in a concentration-dependent manner[1].
Anticancer agent 310 (50-100 μM; 2 h) releases nitric oxide in HGC27 and AGS gastric cancer cells[1].
Anticancer agent 310 (2 μM; 12 h) induces mitochondrial ROS burst in HGC27 and AGS gastric cancer cells[1].
Anticancer agent 310 (2 μM) induces mitochondrial membrane potential depolarization in HGC27 and AGS gastric cancer cells, and this effect is reversed by ROS scavenging[1].
Anticancer agent 310 (2 μM; 36 h) induces apoptosis in HGC27 and AGS gastric cancer cells[1].
Anticancer agent 310 (0.5-2 μM; 24 h) activates the Bax/Bcl-2-Cyt c-Caspase-9/Caspase-3 mitochondrial apoptotic pathway in HGC27 and AGS gastric cancer cells in a dose-dependent manner in vitro[1].
Anticancer agent 310 (0.5-2 μM; 24 h) downregulates SHMT2 and MTHFD2, key enzymes in the folate one-carbon metabolic pathway, in HGC27 and AGS gastric cancer cells in a dose-dependent manner by inhibiting the transcription factor ATF4[1].
Anticancer agent 310 (2 μM; 12 h) disrupts redox homeostasis in HGC27 and AGS gastric cancer cells and reduces the ratios of NADPH/NADP+ and GSH/GSSG[1].

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

Cell Viability Assay[1]

Cell Line: MCF-7, HepG2, HCT-116, HGC27, U251, AGS, ES-2, A2780, K562, MEG01, CT26
Concentration: 0.016, 0.08, 0.4, 2, 5, 10 μM
Incubation Time: 72 h
Result: Exhibited sub-micromolar inhibitory activity across all tested cell lines, with IC50 values as follows: MCF-7: 0.19 μM; HepG2: 0.21 μM; HCT-116: 0.22 μM; HGC27: 0.10 μM; U251: 0.14 μM; AGS: 0.02 μM; ES-2: 0.12 μM; A2780: 0.11 μM; K562: 0.12 μM; MEG01: 0.40 μM; CT26: 0.26 μM.

Apoptosis Analysis[1]

Cell Line: HGC27, AGS
Concentration: 2 μM
Incubation Time: 36 h
Result: Increased total apoptotic cells in HGC27 cells from 10.99% (control) to 83.1%.
Induced a total apoptotic rate of 60.9% in AGS cells.

Western Blot Analysis[1]

Cell Line: HGC27, AGS
Concentration: 0.5, 1, 2 μM
Incubation Time: 24 h
Result: Upregulated the expression of cytoplasmic cytochrome c, Bax, Cleaved Caspase-9, and Cleaved Caspase-3, and downregulated the expression of mitochondrial cytochrome c and Bcl-2 in a dose-dependent manner in both HGC27 and AGS cells.
In Vivo

Anticancer agent 310 (5-15 mg/kg; intratumoral injection; once daily; for 14 consecutive days) exhibits dose-dependent in vivo anti-gastric cancer activity in NCG mice[1].

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

Animal Model: NCG mice treated HGC27 tumor fragments[1]
Dosage: 5 mg/kg; 10 mg/kg; 15 mg/kg
Administration: intratumoral; daily; 14 days
Result: Reduced tumor weight relative to control at 5 mg/kg dose.
Achieved 95.3% tumor growth inhibition (TGI), with 4 out of 6 mice showing complete tumor regression at 10 mg/kg dose.
Achieved 98.78% TGI, with 5 out of 6 mice showing complete tumor regression at 15 mg/kg dose.
Decreased expression of Ki67, SHMT2, and MTHFD2 in tumor tissues relative to control group at 10 mg/kg and 15 mg/kg doses.
Caused no obvious body weight loss or mortality in any dose group.
Molecular Weight

684.71

Formula

C33H36N2O12S

SMILES

O=C1OCC2=C1CC[C@@]3(C)[C@@]2([H])C[C@H]4[C@]5(O4)[C@@]36[C@@H](O6)[C@H](O7)[C@@]7(C(O)(C)C)[C@H]5OC(CCCCOC8=NON=C8S(=O)(C9=CC=CC=C9)=O)=O

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  • 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.

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Anticancer agent 310
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HY-182284
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