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B1793

Sigma-Aldrich

Bafilomycin A1 from Streptomyces griseus

≥90% (HPLC)

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About This Item

Empirical Formula (Hill Notation):
C35H58O9
CAS Number:
88899-55-2
Molecular Weight:
622.83
Beilstein:
4730700
MDL number:
MFCD06795130
UNSPSC Code:
12352200
PubChem Substance ID:
24891613
NACRES:
NA.77

Quality Level

300

Assay

≥90% (HPLC)

form

film

antibiotic activity spectrum

fungi

Mode of action

DNA synthesis | interferes
enzyme | inhibits

storage temp.

−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

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General description

Chemical structure: macrolide

Application

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

Biochem/physiol Actions

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.

Other Notes

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

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

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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
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