assay
~90% (HPLC)
antibiotic activity spectrum
fungi
mode of action
enzyme | inhibits
storage temp.
2-8°C
SMILES string
[H]C(=O)Nc1cccc(C(=O)N[C@H]2[C@@H](C)OC(=O)C(CCCCCC)[C@@H](OC(=O)CC(C)C)[C@H](C)OC2=O)c1O
InChI
1S/C28H40N2O9/c1-6-7-8-9-11-20-25(39-22(32)14-16(2)3)18(5)38-28(36)23(17(4)37-27(20)35)30-26(34)19-12-10-13-21(24(19)33)29-15-31/h10,12-13,15-18,20,23,25,33H,6-9,11,14H2,1-5H3,(H,29,31)(H,30,34)/t17-,18+,20?,23+,25+/m1/s1
InChI key
UIFFUZWRFRDZJC-RBVQMQRASA-N
General description
Chemical structure: peptide
Biochem/physiol Actions
配合物 III的电子转移抑制剂诱导细胞凋亡。
Other Notes
Inhibits the electron transport system
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 2 Oral - Aquatic Acute 1
存储类别
6.1B - Non-combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Faceshields, Gloves, type P2 (EN 143) respirator cartridges
法规信息
新产品
此项目有
G. Hind et al.
Proc. Int. Congr. Photosynth., 4th, D.O. Hall et al., eds., 591-591 (1977)
D Pietrobon et al.
European journal of biochemistry, 117(2), 389-394 (1981-07-01)
The effect of antimycin A and funiculosin, two inhibitors which block electron transfer in the b-c1 complex, on electron flow and electrochemical potential difference of H+ ions in mitochondria at static head (state 4) is investigated. In addition, the respiratory
On the mechanism of inhibition of the respiratory chain by 2-heptyl-4-hydroxyquinoline-N-oxide.
G Izzo et al.
FEBS letters, 93(2), 320-322 (1978-09-15)
Rhianna Williams et al.
Developmental cell, 54(6), 758-772 (2020-08-01)
The loss of protein homeostasis (proteostasis) is a primary driver of age-related tissue dysfunction. Recent studies have revealed that the failure of proteostasis with age is triggered by developmental and reproductive cues that repress the activity of proteostasis-related pathways in
Stephanie A Zlatic et al.
Cell systems, 6(3), 368-380 (2018-02-06)
Rare neurological diseases shed light onto universal neurobiological processes. However, molecular mechanisms connecting genetic defects to their disease phenotypes are elusive. Here, we obtain mechanistic information by comparing proteomes of cells from individuals with rare disorders with proteomes from their
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