Anticancer agent 296
Anticancer agent 296 is a potent anticancer agent that activates the PERK-eIF2α-CHOP signaling pathway to induce endoplasmic reticulum stress, thereby regulating caspase and Bcl-2 family proteins, ultimately leading to apoptosis. Anticancer agent 296 increases intracellular levels of reactive oxygen species (ROS), reduces mitochondrial membrane potential, and promotes Ca2+ release. Anticancer agent 296 suppresses cell colony formation and S-phase cell proliferation, and induces autophagy. Anticancer agent 296 is applicable for research on non-small cell lung cancer (NSCLC).
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- 分子式: C24H22BrF3N2OSi
- 分子量:519.43
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
Anticancer agent 296 (Compound 5b) (1.25-10 μM; 48 h) potently inhibits proliferation of A549 and HeLa cancer cells with IC50 values of 3.88 μM and 3.89 μM, respectively, and has a favorable safety margin against normal cells[1].
Anticancer agent 296 (1.94-3.88 μM; 48 h; 24 h with Mitomycin C (HY-13316) pre-treatment) effectively inhibits migration of A549 cells in a concentration-dependent manner, with 3.88 μM reducing wound healing to 8.19%[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) downregulates FAK protein expression in A549 cells, contributing to inhibited migration, and also activates the PERK-eIF2α-CHOP ER stress pathway and the endogenous apoptotic pathway in A549 cells by regulating key proteins[1].
Anticancer agent 296 (1.94-7.76 μM; 7 days) effectively inhibits colony formation of A549 cells at concentrations ≥3.88 μM[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) activates autophagy in A549 cells by upregulating Beclin-1 and promoting LC3 I/II conversion[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) induces S phase arrest in A549 cells in a dose-dependent manner, with 7.76 μM increasing S phase to 31.33% by downregulating cell cycle-related proteins[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) decreases mitochondrial membrane potential in A549 cells in a concentration-dependent manner[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) increases ROS levels in A549 cells[1].
Anticancer agent 296 (3.88-7.76 μM; 24 h) induces oxidative stress in A549 cells by reducing GSH and increasing MDA levels[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) increases intracellular calcium concentration in A549 cells, with 7.76 μM inducing a 1.68-fold increase[1].
Anticancer agent 296 (3.88 μM; 24 h) induces endoplasmic reticulum stress in A549 cells via the PERK pathway, as evidenced by ER vacuolization[1].
Anticancer agent 296 (1.94-7.76 μM; 24 h) induces early apoptosis in A549 cells, with 7.76 μM increasing early apoptosis to 11.14%[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:A549 (human lung adenocarcinoma), HeLa (human cervical cancer), NIH-3T3 (mouse embryonic fibroblast), THLE-2 (human immortalised liver)
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Concentration:1.25 μM, 2.5 μM, 5 μM and 10 μM
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Incubation Time:48 h
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Result:Potently inhibited proliferation of A549 and HeLa cells with IC50 values of 3.88 μM and 3.89 μM, respectively.
Exhibited lower cytotoxicity against normal cells with IC50 values of 26.48 μM (NIH-3T3) and 12.08 μM (THLE-2).
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Cell Line:A549 cells
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Concentration:1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀)
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Incubation Time:48 h; 24 h (with mitomycin c pre-treatment)
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Result:Reduced scratch healing percentage from 29.31% (control) to 18.16% (1.94 μM) and 8.19% (3.88 μM) after 48 h. Inhibited migration even in the presence of Mitomycin c.
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Cell Line:A549 cells
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Concentration:1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
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Incubation Time:24 h
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Result:Downregulated FAK protein expression compared to the control group.\nUpregulated p53, Bax, cleaved PARP, caspase-3, PERK, GRP78, p-eIF2α, CHOP, STIM1, and ORAI1; downregulated Bcl-2.
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Cell Line:A549 cells
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Concentration:1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
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Incubation Time:24 h
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Result:Increased MDC fluorescence intensity (indicating enhanced autophagy) and upregulated Beclin-1 expression, while p62 decreased and LC3 I/II conversion was observed.
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Cell Line:A549 cells
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Concentration:1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
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Incubation Time:24 h
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Result:Increased S phase percentage from 18.95% (control) to 24.72% (1.94 μM), 27.38% (3.88 μM), and 31.33% (7.76 μM). Reduced expression of Cyclin A2, Cyclin B1, and CDK2.
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Cell Line:A549 cells
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Concentration:1.94 μM (0.5×IC₅₀), 3.88 μM (IC₅₀), 7.76 μM (2×IC₅₀)
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Incubation Time:24 h
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Result:Increased early apoptosis rate from 2.48% (control) to 4.47% (1.94 μM), 9.34% (3.88 μM), and 11.14% (7.76 μM).
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nu mice injected with A549 cells[1]
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Dosage:10 mg/kg; 20 mg/kg
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Administration:i.p.; daily; 12 consecutive days
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Result:Achieved tumor inhibition rates of 62.92% (10 mg/kg) and 80.32% (20 mg/kg). Induced DNA damage in tumor cells with γH2AX positive rates of 60.2% (10 mg/kg) and 69.3% (20 mg/kg). Inhibited tumor proliferation with Ki67 positive rates of 36.5% (10 mg/kg) and 24.4% (20 mg/kg). Observed no significant body weight changes or chronic organ damage.
化学情報
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分子量 519.43
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分子式 C24H22BrF3N2OSi
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SMILES
COC1=CC=CC2=C1C(C(C3=CNC4=CC=C(C=C43)Br)(C(F)(F)F)C#C[Si](C)(C)C)=CN2
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
Anticancer agent 296 関連分類
HY-181087 関連分類
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- Anticancer agent 296
- Anticancer agent296
- Anticancer agent-296
- PERK
- Apoptosis
- Autophagy
- Reactive Oxygen Species (ROS)
- Caspase
- Bcl-2 Family
- HeLa
- PERK-eIF2α-CHOP signaling pathway
- apoptosis
- A549
- non-small cell lung cancer
- lung adenocarcinoma
- reactive oxygen species
- mitochondrial membrane potential
- endoplasmic reticulum stress
- Inhibitor
- inhibitor
- inhibit