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Merck

B1793

Bafilomycin A1

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

Bafilomycin A1 from Streptomyces griseus
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€ 120,00

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€ 351,00

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About This Item

Empirical Formula (Hill Notation):
C35H58O9
CAS Number:
Molecular Weight:
622.83
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
Beilstein/REAXYS Number:
4730700
MDL number:

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Product Name

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

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

assay

≥90% (HPLC)

form

film

antibiotic activity spectrum

fungi

mode of action

DNA synthesis | interferes
enzyme | inhibits

storage temp.

−20°C

Quality Level

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This Item
R0395O487646745
form

film

form

powder

form

powder

form

-

assay

≥90% (HPLC)

assay

≥95% (HPLC)

assay

≥90% total oligomycins basis (HPLC)

assay

-

Quality Level

300

Quality Level

300

Quality Level

200

Quality Level

200

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

storage temp.

2-8°C

antibiotic activity spectrum

fungi

antibiotic activity spectrum

fungi, yeast

antibiotic activity spectrum

fungi

antibiotic activity spectrum

Gram-positive bacteria

mode of action

DNA synthesis | interferes

mode of action

enzyme | inhibits, protein synthesis | interferes

mode of action

enzyme | inhibits

mode of action

protein synthesis | interferes

Application

Bafilomycin A1 has been used:
  • as an autophagy inhibitor to study its effects on hepatic steatosis in human hepatocytes[1]
  • 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[2]
  • as a vacuolar-type H+ -ATPase inhibitor to study its effects on tau degradation in human SH-SY5Y cells[3]

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.[4]
Specific inhibitor of vacuolar type H+-ATPase (V-ATPase).

General description

Chemical structure: macrolide

Storage Class

11 - Combustible Solids

wgk

WGK 3

ppe

dust mask type N95 (US), Eyeshields, Gloves


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ERK-dependent mTOR pathway is involved in berberine-induced autophagy in hepatic steatosis
He Q, et al.
Journal of Molecular Endocrinology, 57(4) (2016)
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
T Yoshimori et al.
The Journal of biological chemistry, 266(26), 17707-17712 (1991-09-15)
Bafilomycin A1 is known as a strong inhibitor of the vacuolar type H(+)-ATPase in vitro, whereas other type ATPases, e.g. F1,F0-ATPase, are not affected by this antibiotic (Bowman, E.M., Siebers, A., and Altendorf, K. (1988) Proc. Natl. Acad. Sci. U.S.A.
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

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We presents an article on Autophagy in Cancer Promotes Therapeutic Resistance

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