콘텐츠로 건너뛰기
Merck

B1793

Sigma-Aldrich

Bafilomycin A1

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

로그인조직 및 계약 가격 보기

크기 선택

제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C35H58O9
CAS 번호:
88899-55-2
Molecular Weight:
622.83
Beilstein:
4730700
MDL number:
MFCD06795130
UNSPSC 코드:
12352200
PubChem Substance ID:
24891613
NACRES:
NA.77

주요 문서

모든 문서 보기
기술 서비스
도움이 필요하신가요? 저희 숙련된 과학자 팀이 도와드리겠습니다.
도움 문의
기술 서비스
도움이 필요하신가요? 저희 숙련된 과학자 팀이 도와드리겠습니다.
도움 문의

제품 이름

Bafilomycin A1 from Streptomyces griseus, ≥90% (HPLC)

Quality Level

300

분석

≥90% (HPLC)

양식

film

항생제 활성 스펙트럼

fungi

동작 모드

DNA synthesis | interferes
enzyme | inhibits

저장 온도

−20°C

SMILES string

CO[C@H]1\C=C\C=C(C)\C[C@H](C)[C@H](O)[C@H](C)\C=C(C)\C=C(OC)C(=O)OC1[C@@H](C)[C@@H](O)[C@H](C)[C@@]2(O)C[C@@H](O)[C@H](C)[C@H](O2)C(C)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

유사한 제품을 찾으십니까? 방문 제품 비교 안내

관련 카테고리

일반 설명

Chemical structure: macrolide

애플리케이션

Bafilomycin A1 has been used:
  • as an autophagy inhibitor to study its effects on hepatic steatosis in human hepatocytes
  • as a vacuolar-type H+ -ATPase inhibitor to study its effects on the cell viability, percentage of PI-positive cells, and glucose-stimulated insulin secretion (GSIS) in mice INS-1 cells
  • as a vacuolar-type H+ -ATPase inhibitor to study its effects on tau degradation in human SH-SY5Y cells

생화학적/생리학적 작용

A specific inhibitor of vacuolar type H+-ATPase (V-ATPase) in animal cells, plant cells and microorganisms.
Bafilomycin A1 inhibits autophagosome-lysosome fusion and autolysosome acidification, the steps involved in the autophagic process that is required for maintaining functional autophagic flux and cellular homeostasis.
Specific inhibitor of vacuolar type H+-ATPase (V-ATPase).

기타 정보

2024 CiteAb Award Winner for Supplier Succeeding in Parkinson′s Research

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

개인 보호 장비

dust mask type N95 (US), Eyeshields, Gloves

가장 최신 버전 중 하나를 선택하세요:

시험 성적서(COA)

Lot/Batch Number
089M4007V
099M4001V
14190116
108M4123V
14180908

적합한 버전을 찾을 수 없으신가요?

특정 버전이 필요한 경우 로트 번호나 배치 번호로 특정 인증서를 찾을 수 있습니다.

COA 검색

이 제품을 이미 가지고 계십니까?

문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

Jens Niewoehner et al.
Neuron, 81(1), 49-60 (2014-01-15)
Although biotherapeutics have vast potential for treating brain disorders, their use has been limited due to low exposure across the blood-brain barrier (BBB). We report that by manipulating the binding mode of an antibody fragment to the transferrin receptor (TfR)
T Umata et al.
The Journal of biological chemistry, 265(35), 21940-21945 (1990-12-15)
The role of vacuolar-type H(+)-ATPase (V-ATPase) in the cytotoxic action of diphtheria toxin (DT) was studied by using bafilomycin A1, a specific inhibitor of V-ATPase. Studies with acridine orange showed that the acidification of intracellular acidic compartments was inhibited strongly
Ru Li et al.
Phytopathology, 109(8), 1417-1424 (2019-03-13)
The vacuolar H+-ATPases (V-ATPases) are conserved ATP-dependent proton pumps that acidify intracellular compartments in eukaryotic cells. The role of Cpvma1, a V-ATPase catalytic subunit A of Cryphonectria parasitica, was investigated by generating cpvma1-overexpressing and cpvma1-silenced strains. The mutant strains were
Feng-Xia Guo et al.
Cell death and differentiation, 26(9), 1670-1687 (2019-01-27)
Atherosclerosis is a progressive, chronic inflammation in arterial walls. Long noncoding RNAs (lncRNAs) participate in inflammation, but the exact mechanism in atherosclerosis is unclear. Our microarray analyses revealed that the levels of lncRNA-FA2H-2 were significantly decreased by oxidized low-density lipoprotein
Kun Wang et al.
International journal of molecular sciences, 20(14) (2019-07-25)
The main mechanistic function of most chemotherapeutic drugs is mediated by inducing mitochondria-dependent apoptosis. Tumor cells usually respond to upregulate autophagy to eliminate impaired mitochondria for survival. Hypothetically, inhibiting autophagy might promote mitochondria-dependent apoptosis, thus enhancing the efficacy of chemotherapeutic
모든 관련된 서류 보기

문서

Autophagy in Cancer Promotes Therapeutic Resistance

We presents an article on Autophagy in Cancer Promotes Therapeutic Resistance

관련 콘텐츠

자사의 과학자팀은 생명 과학, 재료 과학, 화학 합성, 크로마토그래피, 분석 및 기타 많은 영역을 포함한 모든 과학 분야에 경험이 있습니다..

고객지원팀으로 연락바랍니다.