021-51111890
购物车（）
sales@molnova.cn
SP-8356
CAS No. 1454885-45-0
SP-8356 ( —— )
产品货号. M26459 CAS No. 1454885-45-0
SP-8356 is a potent, orally active inhibitor of cluster of differentiation 147 (CD147) with anti-atherosclerotic effects.
纯度: >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| 规格 | 价格/人民币 | 库存 | 数量 |
| 5MG | ￥2130 | 有现货 |
|
| 10MG | ￥3378 | 有现货 |
|
| 25MG | ￥6383 | 有现货 |
|
| 50MG | ￥8667 | 有现货 |
|
| 100MG | ￥11583 | 有现货 |
|
| 500MG | ￥23409 | 有现货 |
|
| 1G | 获取报价 | 有现货 |
|
生物学信息
-
产品名称SP-8356
-
注意事项本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断
-
产品简述SP-8356 is a potent, orally active inhibitor of cluster of differentiation 147 (CD147) with anti-atherosclerotic effects.
-
产品描述SP-8356 is a potent, orally active inhibitor of cluster of differentiation 147 (CD147) with anti-atherosclerotic effects.(In Vitro):In a time- and dose-dependent manner, SP-8356 (5-10?μM; 48 hours) inhibits the growth of various types of breast cancer cell lines. SP-8356 (10?μM; 48 hours) increases the percentage of MDA-MB231 cells in the S phase and decreases caspase-3 and cleaved PARP .(In Vivo):In a xenograft mouse model, SP-8356 (10?mg/kg; i.p.; every three days until the 42nd day) inhibits tumor growth . SP-8356 (50 mg/kg; p.o.; daily one day after carotid artery ligation for three weeks) prevents the formation of plaque and attenuates its vulnerability .
-
同义词——
-
通路Autophagy
-
靶点Autophagy
-
受体COX-2; ROS
-
研究领域——
-
适应症——
化学信息
-
CAS Number1454885-45-0
-
分子量300.4
-
分子式C18H20O4
-
纯度>98% (HPLC)
-
溶解度——
-
SMILES[H][C@@]12C[C@@]([H])(C(\C=C\c3cc(O)c(O)c(OC)c3)=CC1=O)C2(C)C
-
化学全称——
运输与储存
-
储存条件(-20℃)
-
运输条件With Ice Pack
-
稳定性≥ 2 years
参考文献
1.Zhenggang Zhou, et al. PBN Protects NP Cells From AAPH-induced Degenerative Changes by Inhibiting the ERK1/2 Pathway. Connect Tissue Res. 2020 Mar 30;1-10.
产品手册
关联产品
-
O4I1
O4I1 is an effective Oct3/4 inducer.
-
Sulfanilamide
Sulfanilamide is a competitive inhibitor for bacterial enzymedihydropteroate synthetasewithIC50of 320 μM.
-
Sulfuretin
Sulfuretin is a potent anti-oxidant, has protective effect against t-BHP-induced oxidative damage in human liver-derived HepG2 cells is attributable to its ability to scavenge ROS and up-regulate the activity of HO-1 through the Nrf2/ARE and JNK/ERK signaling pathways.
