262017
APE1 Inhibitor III
The APE1 Inhibitor III controls the biological activity of APE1. This small molecule/inhibitor is primarily used for Cell Structure applications.
同義詞:
APE1 Inhibitor III, Apurinic Endonuclease 1 Inhibitor III, Apurinic/Apyrimidinic Endonuclease 1 Inhibitor III, N-(3-(1,3-Benzo[d]thiazol-2-yl)-6-isopropyl-4,5,6,7-tetrahydrothieno[2,3-c]pyridin-2-yl)acetamide, N-(3-(1,3-Benzo[d]thiazol-2-yl)-6-isopropyl-4,5,6,7-tetrahydrothieno[2,3-c]pyridin-2-yl)acetamide, Apurinic Endonuclease 1 Inhibitor III, Apurinic/Apyrimidinic Endonuclease 1 Inhibitor III
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About This Item
推薦產品
品質等級
化驗
≥95% (HPLC)
形狀
solid
製造商／商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
brown
溶解度
DMSO: 2.5 mg/mL
運輸包裝
ambient
儲存溫度
2-8°C
SMILES 字串
CC(C)N(CC1)CC2=C1C(C3=NC4=C(C=CC=C4)S3)=C(S2)NC(C)=O
一般說明
A cell-permeable benzothiazolyltetrahydrothienopyridine compound that acts as a potent, competitive, and active site targeting inhibitor of APE1 (IC50 = 2.0 µM in a fluorescence based HTS assay; and 12 .0 µM in a radiotracer incision assay). Shown to block APE1 activity in HEK293T and HeLa cells extract (IC50 = 600 nM) and increase genomic AP site accumulation. Potentiates the cytotoxicity of DNA-damaging alkylating agents in HeLa cells by ~3-fold. Exhibits favorable pharmacokinetic properties and desirable ADME attributes. Due to its lipophilic nature, it crosses the blood-brain barrier rather easily and shows desirable stability (t1/2 = 80 min).
生化／生理作用
Cell permeable: yes
Primary Target
APE1
APE1
Reversible: yes
包裝
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重構
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他說明
Rai, G., et al. 2012. J. Med. Chem.55, 3101.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 2
閃點（°F）
Not applicable
閃點（°C）
Not applicable
分析證明 (COA)
輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號，寫有 ‘Lot’或‘Batch’.。
J-L Yang et al.
Neuropathology and applied neurobiology, 46(4), 375-390 (2019-10-20)
Accumulating studies have suggested that base excision repair (BER) is the major repair pathway of oxidative DNA damage in neurons, and neurons are deficient in other DNA repair pathways, including nucleotide excision repair and homologous recombination repair. However, some studies
Huimin Zhang et al.
Nature communications, 13(1), 4240-4240 (2022-07-23)
Anticancer drugs, such as camptothecin (CPT), trap topoisomerase I (TOP1) on DNA and form TOP1 cleavage complexes (TOP1cc). Alternative repair pathways have been suggested in the repair of TOP1cc. However, how these pathways work with TDP1, a key repair enzyme
Mrinal Srivastava et al.
EMBO reports, 21(6), e49123-e49123 (2020-04-21)
Replication across oxidative DNA lesions can give rise to mutations that pose a threat to genome integrity. How such lesions, which escape base excision repair, get removed without error during replication remains unknown. Our PCNA-based screen to uncover changes in
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