>>Signaling Pathways>> Apoptosis>> Other Apoptosis>>ROC-325

ROC-325

Catalog No.GC32901

ROC-325는 강력한 항암 활성을 가진 강력한 경구 활성 자가포식 억제제입니다. ROC-325는 리소좀의 탈산성화, 자가포식소체 축적 및 자가포식 플럭스 방해를 유도합니다. ROC-325는 또한 신세포 암종 세포자멸사를 유도합니다.

Products are for research use only. Not for human use. We do not sell to patients.

ROC-325 Chemical Structure

Cas No.: 1859141-26-6

Size 가격 재고 수량
10mM (in 1mL DMSO)
US$112.00
재고 있음
5mg
US$101.00
재고 있음
10mg
US$157.00
재고 있음
25mg
US$313.00
재고 있음
50mg
US$506.00
재고 있음
100mg
US$911.00
재고 있음

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Sample solution is provided at 25 µL, 10mM.

Description Protocol Chemical Properties Product Documents Related Products

ROC-325 is a novel inhibitor of autophagy.

ROC-325 is a novel inhibitor of autophagy. Treatment with ROC-325 results in a significant loss of acridine orange fluorescence. ROC-325 triggers a highly significant increase in cathepsin D (CTSD) levels. ROC-325 treatment yields pharmacodynamic effects that are consistent with inhibition of autophagy. Treatment with 5 μM ROC-325 for 24 hours leads to the formation of LC3B punctae and a robust increase in LC3B levels in both A498 and 786-0 RCC cells. Immunoblotting analysis conducted in both A498 and 786-0 cells demonstrates that ROC-325 promotes a dose-dependent increase in LC3B expression in a manner that correlated with a corresponding increase in the levels of p62 and cathepsin D[1].

ROC-325 treatment leads to significant, dose-dependent inhibition of disease progression. ROC-325 is well tolerated and no notable toxicities are observed other than a very modest, nonsignificant reduction in mean body weight at the highest dose. Immunohistochemical analysis of specimens collected from animals treated with ROC-325 demonstrates significant, dose-dependent increases in the autophagic markers LC3B and p62 and increases apoptosis[1].

[1]. Carew JS, et al. Disruption of Autophagic Degradation with ROC-325 Antagonizes Renal Cell Carcinoma Pathogenesis. Clin Cancer Res. 2017 Jun 1;23(11):2869-2879.

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Average Rating: 5 ★★★★★ (Based on Reviews and 20 reference(s) in Google Scholar.)

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