ADTL-SA1215
目录号 : GC64527
ADTL-SA1215 是一种调节三阴性乳腺癌自噬的特异性 SIRT3 小分子激活剂。
Cas No.:782387-91-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
ADTL-SA1215 is a first-in-class specific small-molecule activator of SIRT3 that modulates autophagy in triple negative breast cancer.
[1]. Zhang J, et al. Structure-Guided Design of a Small-Molecule Activator of Sirtuin-3 that Modulates Autophagy in Triple Negative Breast Cancer. J Med Chem. 2021 Oct 14;64(19):14192-14216.
| Cas No. | 782387-91-1 | SDF | Download SDF |
| 分子式 | C26H29I2NO3 | 分子量 | 657.32 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5213 mL | 7.6066 mL | 15.2133 mL |
| 5 mM | 0.3043 mL | 1.5213 mL | 3.0427 mL |
| 10 mM | 0.1521 mL | 0.7607 mL | 1.5213 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Structure-Guided Design of a Small-Molecule Activator of Sirtuin-3 that Modulates Autophagy in Triple Negative Breast Cancer
J Med Chem 2021 Oct 14;64(19):14192-14216.PMID:34605238DOI:10.1021/acs.jmedchem.0c02268
Sirtuin-3 (SIRT3) is an NAD+-dependent protein deacetylase localized primarily in the mitochondria with many links to different types of human cancers. Autophagy, which is a highly conserved lysosomal degradation process in eukaryotic cells, has been recently reported to be positively regulated by SIRT3 in cancer; therefore, activating SIRT3-modulated autophagy may be a promising strategy for drug discovery. In this study, we discovered a small-molecule activator of SIRT3 compound 33c (ADTL-SA1215) with specific SIRT3 deacetylase activity by structure-guided design and high-throughput screening. Subsequently, compound 33c inhibited the proliferation and migration of human breast carcinoma MDA-MB-231 cells by SIRT3-driven autophagy/mitophagy signaling pathways in vitro and in vivo. Collectively, these results demonstrate that pharmacological activation of SIRT3 is a potential therapeutic approach of triple negative breast cancer (TNBC). More importantly, compound 33c may be a first-in-class specific small-molecule activator of SIRT3 that would be utilized for future cancer drug development.