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Merck
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安全性情報

196000

Sigma-Aldrich

Bafilomycin A1

from Streptomyces griseus, ≥90% (HPLC), film, V-ATPase inhibitor, Calbiochem

別名:

Bafilomycin A1, Streptomyces griseus

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About This Item

実験式（ヒル表記法）:
C35H58O9
CAS番号:
88899-55-2
分子量:
622.83
MDL番号:
MFCD06795130
UNSPSCコード:
12352200
NACRES:
NA.77

product name

Bafilomycin A1, Streptomyces griseus, Bafilomycin A1, CAS 88899-55-2, acts as a highly potent and specific inhibitor of vacuolar-type H+-ATPase (Ki = 500 pM). Blocks the fusion of autophagosome with lysosome.

品質水準

100

アッセイ

≥90% (HPLC)

形状

film

シェルフライフ

3 yr

メーカー／製品名

Calbiochem®

保管条件

OK to freeze
protect from light

溶解性

DMSO: 100 μM
ethanol: soluble

保管温度

−20°C

InChI

1S/C35H58O9/c1-19(2)32-24(7)27(36)18-35(40,44-32)26(9)31(38)25(8)33-28(41-10)14-12-13-20(3)15-22(5)30(37)23(6)16-21(4)17-29(42-11)34(39)43-33/h12-14,16-17,19,22-28,30-33,36-38,40H,15,18H2,1-11H3/b14-12+,20-13+,21-16+,29-17-/t22-,23+,24-,25-,26-,27+,28-,30-,31+,32+,33+,35+/m0/s1

InChI Key

XDHNQDDQEHDUTM-JQWOJBOSSA-N

詳細

A macrolide antibiotic that acts as a specific inhibitor of vacuolar-type H+-ATPase (V-type; Ki = 500 pM). A valuable tool for distinguishing among different types of ATPases. Blocks lysosomal cholesterol trafficking in macrophages and is known to interfere with pH regulation in brain cells. Exhibits cytotoxic effects on a number of cell lines in a cell viability assay. Reported to selectively inhibit β-secretase, an enzyme involved in the processing of amyloid precursor protein (APP). The InSolution format with a purity of ≥97% by HPLC in 90% DMSO is also available (Cat. No. 508409).
Note: 1 set = 3 x 10 µg

生物化学的／生理学的作用

Primary Target
vacuolar type H+ ATPase

警告

Toxicity: Carcinogenic / Teratogenic (D)

再構成

Following reconstitution, aliquot and freeze (-20°C). DMSO stock solutions are stable for up to 1 year at -20°C.

その他情報

Sinha, S., and Lieberburg, I. 1999. Proc. Natl. Acad. Sci. USA96, 11049.
Calvert, C.M., and Sanders, D. 1995. J. Biol. Chem.270, 7272.
Nishihara, T., et al. 1995. Biochem. Biophys. Res. Commun.269, 255.
Crider, B.P., et al. 1994. J. Biol. Chem.269, 17379.
Palokangas, H., et al. 1994. J. Biol. Chem.269, 17577.
Sundquist, K.T., and Marks, S.C., Jr. 1994. J. Bone Miner. Res.9, 1575.
Drose, S., et al. 1993. Biochemistry32, 3902.
Furuchi, T., et al. 1993. J. Biol. Chem.268, 27345.
Bowman, E.J., et al. 1988. Proc. Natl. Acad. Sci. USA85, 7972.

法的情報

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

保管分類コード

11 - Combustible Solids

WGK

WGK 3

適用法令

試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。

Jan Code

R2951:
196000-10LUG:
196000-10UG:
196000-1SET:
196000-UG:

試験成績書（COA）

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Sigma-Aldrich

Sigma-Aldrich

SAE0107

3-Methyladenine Ready made solution

ブチルベンゼン analytical standard

Supelco

19600

ブチルベンゼン

3-Methyl-d3-adenine ≥98 atom % D, ≥98% (CP)

Sigma-Aldrich

900525

3-Methyl-d3-adenine

Rapamycin ≥95% (HPLC), powder

Sigma-Aldrich

553210

Rapamycin

(+)-Brefeldin A, Eupenicillium brefeldianum Specifically and reversibly blocks translocation of proteins from the endoplasmic reticulum (ER) to the Golgi apparatus without affecting endocytosis or lysosome function.

Sigma-Aldrich

203729

(+)-Brefeldin A, Eupenicillium brefeldianum

Cycloheximide InSolution, ≥98%

Millipore

5.08739

Cycloheximide

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Oxidative medicine and cellular longevity, 2020, 9595036-9595036 (2020-07-21)
Subendothelial retention of apolipoprotein B100-containing lipoprotein, such as low-density lipoprotein (LDL), is the initial step of atherogenesis. Activation of autophagy exhibits beneficial effects for the treatment of atherosclerosis. In our previous study, we demonstrated that hyperglycemia suppressed autophagic degradation of
Joaquim Bosch-Barrera et al.
Cancers, 13(16) (2021-08-28)
The anti-angiogenic agent nintedanib has been shown to prolong overall and progression-free survival in patients with advanced non-small-cell lung cancer (NSCLC) who progress after first-line platinum-based chemotherapy and second-line immunotherapy. Here, we explored the molecular basis and the clinical benefit
Yulan Liu et al.
Diabetes & vascular disease research, 19(3), 14791641221102513-14791641221102513 (2022-05-14)
This study aims to determine the role and mechanism of autophagy in endothelial cell dysfunction by glucolipotoxicity. Human umbilical vein endothelial cells (HUVECs) were treated with high glucose and high palmitic acid. The number of autophagosomes was evaluated by monodansylcadaverine
Lynne Chantranupong et al.
eLife, 9 (2020-10-13)
Neurons communicate by the activity-dependent release of small-molecule neurotransmitters packaged into synaptic vesicles (SVs). Although many molecules have been identified as neurotransmitters, technical limitations have precluded a full metabolomic analysis of SV content. Here, we present a workflow to rapidly
Yixuan Fang et al.
Aging cell, 19(10), e13232-e13232 (2020-09-21)
Autophagy suppresses mitochondrial metabolism to preserve hematopoietic stem cells (HSCs) in mice. However, the mechanism by which autophagy regulates hematopoietic aging, in particular in humans, has largely been unexplored. Here, we demonstrate that reduction of autophagy in both hematopoietic cells
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