epi-Avermectin B1a
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| Category | Bioactive by-products |
| Catalog number | BBF-04207 |
| CAS | 106434-14-4 |
| Molecular Weight | 873.08 |
| Molecular Formula | C48H72O14 |
| Purity | >95% by HPLC |
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Description
It is a base-catalysed intermediate in the decomposition of avermectin B1a. It has only very weak activity as a nematocide showing 100-fold less of biological activity compared with the parent avermectin. It is an environmental degradation product.
Specification
| Synonyms | Avermectin B1a, epi-; 2-epi-Abamectin; (2S)-5-O-demethyl-avermectin A1a |
| Storage | Store at -20°C |
| IUPAC Name | (1'S,2R,3S,4'S,6S,8'R,10'E,12'S,13'S,14'E,16'E,20'R,21'R,24'S)-2-[(2S)-butan-2-yl]-21',24'-dihydroxy-12'-[(2R,4S,5S,6S)-5-[(2S,4S,5S,6S)-5-hydroxy-4-methoxy-6-methyloxan-2-yl]oxy-4-methoxy-6-methyloxan-2-yl]oxy-3,11',13',22'-tetramethylspiro[2,3-dihydropyran-6,6'-3,7,19-trioxatetracyclo[15.6.1.14,8.020,24]pentacosa-10,14,16,22-tetraene]-2'-one |
| Canonical SMILES | CCC(C)C1C(C=CC2(O1)CC3CC(O2)CC=C(C(C(C=CC=C4COC5C4(C(C=C(C5O)C)C(=O)O3)O)C)OC6CC(C(C(O6)C)OC7CC(C(C(O7)C)O)OC)OC)C)C |
| InChI | InChI=1S/C48H72O14/c1-11-25(2)43-28(5)17-18-47(62-43)23-34-20-33(61-47)16-15-27(4)42(26(3)13-12-14-32-24-55-45-40(49)29(6)19-35(46(51)58-34)48(32,45)52)59-39-22-37(54-10)44(31(8)57-39)60-38-21-36(53-9)41(50)30(7)56-38/h12-15,17-19,25-26,28,30-31,33-45,49-50,52H,11,16,20-24H2,1-10H3/b13-12+,27-15+,32-14+/t25-,26-,28-,30-,31-,33+,34-,35+,36-,37-,38-,39-,40+,41-,42-,43+,44-,45+,47+,48+/m0/s1 |
| InChI Key | RRZXIRBKKLTSOM-TYECJXEWSA-N |
| Source | Semi-synthetic |
Properties
| Appearance | White Solid |
| Antibiotic Activity Spectrum | Parasites |
| Boiling Point | 940.9±65.0°C at 760 mmHg |
| Density | 1.2±0.1 g/cm3 |
| Solubility | Soluble in Ethanol, Methanol, DMF, DMSO |
Reference Reading
1. Bioaccumulation and elimination of avermectin B1a in the earthworms (Eisenia fetida)
Jianzhong Shen, Xiaoping Diao, Qidi Zhang, Yingjian Sun Chemosphere . 2005 Jul;60(5):699-704. doi: 10.1016/j.chemosphere.2005.01.044.
The acute toxicity, bioaccumulation, and elimination of avermectin B1a (AVM B1a) in earthworm (Eisenia fetida) were investigated in different exposure systems. The LC50 of AVM B1a on earthworms were 24.1 mg/kg and 17.1 mg/kg, respectively, for 7 and 14 days in artificial soil. The LC50 tested by the filter paper for 2 days was 4.63 microg/cm2. The earthworms were cultivated in artificial soil containing 0.6 mg/kg and 3.0 mg/kg AVM B1a, respectively for bioaccumulation experiments. The AVM B1a residues in earthworms were determined with HPLC-fluorescence method. The results showed that AVM B1a was taken up from the concentrated artificial soil by the earthworms and the steady-state levels were reached after 9-18 days of exposure. On the 18th day, the final concentrations of AVM B1a in the earthworms treated with two different dosages were 107 ng/g and 165 ng/g, respectively; there were not significantly accumulation. About 80.0% and 94.8% of the accumulated AVM B1a were eliminated respectively in two groups within 1 day after they were exposed to AVM B1a-free soil, but a trace amount of AVM B1a was found for a relative long time in earthworms.
2. Avermectin B1a modulation of gamma-aminobutyric acid receptors in rat brain membranes
S S Pong, C C Wang J Neurochem . 1982 Feb;38(2):375-9. doi: 10.1111/j.1471-4159.1982.tb08639.x.
Avermectin B1a stimulates high-affinity binding of [3H]-gamma-aminobutyric acid (GABA) to receptors in washed rat brain membranes. Scatchard analysis of the data indicates that the drug does not significantly alter the apparent dissociation constant of GABA binding, but increases the detectable number of binding sites from 3.2 to 5.1 pmol/mg protein, (+)-Bicuculline completely blocks control and avermectin B1a-stimulated GABA binding, whereas picrotoxin antagonizes specifically the avermectin B1a-stimulated GABA binding. The avermectin B1a-stimulated GABA binding is also chloride ion-dependent, whereas GABA binding in the control is not. These observations suggest that the mechanism of avermectin B1a stimulation of GABA binding may involve the chloride ion channel.
3. Avermectin B1a production in Streptomyces avermitilis is enhanced by engineering aveC and precursor supply genes
Yanting You, Ying Wen, Gang Liu, Yi Hao, Zhi Chen, Jilun Li Appl Microbiol Biotechnol . 2022 Mar;106(5-6):2191-2205. doi: 10.1007/s00253-022-11854-w.
Avermectins (AVEs) are economically potent anthelmintic agents produced by Streptomyces avermitilis. Among eight AVE components, B1a exhibits the highest insecticidal activity. The purpose of this study was to enhance B1a production, particularly in the high-yielding industrial strain A229, by a combination strategy involving the following steps. (i) aveC gene was engineered to increase B1a:B2a ratio. Three aveC variants (aveC2m, aveC5m, and aveC8m, respectively encoding two, five, and eight amino acid mutations) were synthesized by fusion PCR. B1a:B2a ratio in A229 derivative having kasOp*-controlled aveC8m reached 1.33 (B1a and B2a titers were 8120 and 6124 μg/mL). Corresponding values in A229 were 0.99 and 6447 and 6480 μg/mL. (ii) β-oxidation pathway genes fadD and fadAB were overexpressed in wild-type (WT) strain and A229 to increase supply of acyl-CoA precursors for AVE production. The resulting strains all showed increased B1a titer. Co-overexpression of pkn5p-driven fadD and fadAB in A229 led to B1a titer of 8537 μg/mL. (iii) Genes bicA and ecaA involved in cyanobacterial CO2-concentrating mechanism (CCM) were introduced into WT and A229 to enhance carboxylation velocity of acetyl-CoA and propionyl-CoA carboxylases, leading to increased supply of malonyl- and methylmalonyl-CoA precursors and increased B1a titer. Co-expression of bicA and ecaA in A229 led to B1a titer of 8083 μg/mL. (iv) aveC8m, fadD-fadAB, and bicA-ecaA were co-overexpressed in A229, resulting in maximal B1a titer (9613 μg/mL; 49.1% increase relative to A229). Our findings demonstrate that the combination strategy we provided here is an efficient approach for improving B1a production in industrial strains.Key points· aveC mutation increased avermectin B1a:B2a ratio and B1a titer.· Higher levels of acyl-CoA precursors contributed to enhanced B1a production.· B1a titer in an industrial strain was increased by 49.1% via a combination strategy.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
