2. Cell Cycle/DNA Damage Apoptosis Anti-infection
  3. Topoisomerase DNA/RNA Synthesis Checkpoint Kinase (Chk) Apoptosis Bacterial
  4. 4"-Isovalerylspiramycin I

4"-Isovalerylspiramycin I  (Synonyms: Isovalerylspiramycin I; Shengjimycin E)

目录号: HY-N15249
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4"-Isovalerylspiramycin I (Isovalerylspiramycin I) 是一种拓扑异构酶 1 (TOP1) 抑制剂和抗肿瘤剂。4"-Isovalerylspiramycin I 可直接结合 TOP1，抑制 DNA 复制并诱导 DNA 损伤。4"-Isovalerylspiramycin I 可下调磷酸化 CHEK1 及 ATR/CHEK1 DNA 损伤修复通路，阻断 DNA 修复并加重 DNA 损伤。4"-Isovalerylspiramycin I 可抑制骨肉瘤细胞的增殖、迁移及侵袭。4"-Isovalerylspiramycin I 可诱导骨肉瘤细胞凋亡 (apoptosis) 及细胞周期阻滞。4"-Isovalerylspiramycin I 对耐甲氧西林金黄色葡萄球菌具有抗菌活性。4"-Isovalerylspiramycin I 可用于骨肉瘤、上呼吸道细菌感染及耐甲氧西林金黄色葡萄球菌感染的研究。

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4

4"-Isovalerylspiramycin I Chemical Structure

CAS No. : 267662-22-6

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4"-Isovalerylspiramycin I 相关抗体

Top Publications Citing Use of Products

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

4"-Isovalerylspiramycin I (Isovalerylspiramycin I) is a topoisomerase 1 (TOP1) inhibitor and an antitumor agent. 4"-Isovalerylspiramycin I directly binds to TOP1, suppresses DNA replication, and induces DNA damage. 4"-Isovalerylspiramycin I downregulates phosphorylated CHEK1 and the ATR/CHEK1 DNA damage repair pathway, blocks DNA repair, and augments DNA damage. 4"-Isovalerylspiramycin I suppresses proliferation, migration, and invasion of osteosarcoma cells. 4"-Isovalerylspiramycin I induces apoptosis and cell cycle arrest in osteosarcoma cells. 4"-Isovalerylspiramycin I exerts antibacterial activity against methicillin-resistant Staphylococcus aureus. 4"-Isovalerylspiramycin I can be used for the research of osteosarcoma, upper respiratory bacterial infections, and methicillin-resistant Staphylococcus aureus infection[1][2].

IC50 & Target[1]

Top1

 

Chk1

 

体外研究
(In Vitro)

4"-Isovalerylspiramycin I (0-50 µM；24 h) 在孵育 24 小时后可剂量依赖性地抑制 143B 和 Saos-2 人骨肉瘤细胞的增殖，其 IC50 值分别为 8.7 µM 和 17.8 µM；TOP1 过表达可逆转该作用[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h) 以剂量依赖的方式抑制 143B 和 Saos-2 人骨肉瘤细胞在孵育 24 小时后的迁移能力；该作用可通过 TOP1 过表达逆转[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h pre-treatment) 可呈剂量依赖性地抑制 143B 和 Saos-2 人骨肉瘤细胞的侵袭能力[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h) 经 24 小时孵育后，可在人骨肉瘤细胞 143B 和 Saos-2 中剂量依赖性地抑制 DNA 复制，该效应通过 EdU 掺入量减少得以验证[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h) 在孵育 24 小时后，可剂量依赖性地诱导人骨肉瘤细胞系 143B 和 Saos-2 发生细胞凋亡[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h) 以剂量依赖的方式改变 143B 和 Saos-2 人骨肉瘤细胞中促凋亡和抗凋亡蛋白的表达，孵育时间为 24 小时[1]。
4"-Isovalerylspiramycin I (2.5-20 µM; 24 h) 经 24 小时孵育后，可在人骨肉瘤细胞 143B 和 Saos-2 中呈剂量依赖性下调 G0/G1 细胞周期调控蛋白的表达[1]。
4"-Isovalerylspiramycin I (10-20 µM; 18 h) 可直接与 143B 和 Saos-2 人骨肉瘤细胞中的细胞内 TOP1 结合，在孵育 18 小时后提高 TOP1 的热稳定性[1]。
4"-Isovalerylspiramycin I (0.125 μg/ml) 对耐甲氧西林金黄色葡萄球菌 Staphylococcus aureus CMCC 5342 具有抑制作用，其 MIC 为 0.125 μg/mL[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

4"-Isovalerylspiramycin I 相关抗体:

Cell Proliferation Assay[1]

Cell Line: 143B and Saos-2
Concentration: 0-40 µM (143B, TOP1-overexpressing 143B); 0-50 µM (Saos-2, TOP1-overexpressing Saos-2)
Incubation Time: 24 h
Result: Inhibited 143B and Saos-2 cell proliferation in a dose- and time-dependent manner, with IC50 values of 8.7 µM (143B) and 17.8 µM (Saos-2) after 24 h.
Increased IC50 values to 19.2 µM (TOP1-overexpressing 143B) and 30.6 µM (TOP1-overexpressing Saos-2) after 24 h, reversing the antiproliferative effect.

Cell Migration Assay[1]

Cell Line: 143B and Saos-2
Concentration: 2.5-10 µM (143B); 5-20 µM (Saos-2)
Incubation Time: 24 h
Result: Reduced wound closure in both 143B and Saos-2 cells in a dose-dependent manner, inhibiting cell migration.
Reversed this inhibitory effect on migration when TOP1 was overexpressed.

Cell Invasion Assay[1]

Cell Line: 143B and Saos-2
Concentration: 2.5-10 µM (143B); 5-20 µM (Saos-2)
Incubation Time: 24 h (pre-treatment)
Result: Reduced the number of invading 143B and Saos-2 cells in a dose-dependent manner.
Reversed this inhibitory effect on invasion when TOP1 was overexpressed.

Apoptosis Analysis[1]

Cell Line: 143B and Saos-2
Concentration: 2.5-10 µM (143B); 5-20 µM (Saos-2)
Incubation Time: 24 h
Result: Induced dose-dependent apoptosis in both 143B and Saos-2 cells, with apoptosis rates reaching ~30% (143B at 10 µM) and ~30% (Saos-2 at 20 µM).

Western Blot Analysis[1]

Cell Line: 143B and Saos-2
Concentration: 2.5-10 µM (143B); 5-20 µM (Saos-2)
Incubation Time: 24 h
Result: Downregulated BCL-2 protein expression and upregulated cleaved caspase-3 and BAX protein expression in both 143B and Saos-2 cells in a dose-dependent manner.
Reduced protein expression of CDK4 and Cyclin D1 in both 143B and Saos-2 cells in a dose-dependent manner.

Cell Cycle Analysis[1]

Cell Line: 143B and Saos-2
Concentration: 2.5-10 µM (143B); 5-20 µM (Saos-2)
Incubation Time: 24 h
Result: Induced a dose-dependent increase in the percentage of cells in the G0/G1 phase, with a corresponding decrease in the S-phase population in both 143B and Saos-2 cells.
体内研究
(In Vivo)

4"-Isovalerylspiramycin I (Isovalerylspiramycin I) (60 mg/kg; i.p.; every 1 day; 30 days) 可显著抑制雌性 M-NSG 小鼠的皮下骨肉瘤肿瘤生长与肺转移，且耐受性良好[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: M-NSG mice (female, 4-6 weeks old, ~20 g) injected with 143B cells.[1]
Dosage: 60 mg/kg
Administration: i.p.; every 1 day; 30 days
Result: Significantly inhibited increases in tumor volume in 143B xenografts.
Showed no significant difference in mouse body weight compared to controls, indicating good tolerability.
Reduced TOP1 expression in tumor tissues via immunohistochemical staining.
Significantly inhibited osteosarcoma lung metastasis via lung H&E staining.
分子量

927.17

Formula

C48H82N2O15
CAS 号
结构分类
初始来源

S. spiramyceticus F21
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

4"-Isovalerylspiramycin I 相关分类

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Keywords:

4"-Isovalerylspiramycin I267662-22-6Isovalerylspiramycin I Shengjimycin ETopoisomeraseDNA/RNA SynthesisCheckpoint Kinase (Chk)ApoptosisBacterialTOP1osteosarcoma cellsCHEK1methicillin-resistant Staphylococcus aureusapoptosisATR/CHEK1 pathwayDNA replicationtumour xenograft mouse modelDNA damagecell cycle arrestInhibitorinhibitorinhibit

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