epi-Ivermectin B1a
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Others |
| Catalog number | BBF-04259 |
| CAS | |
| Molecular Weight | 875.09 |
| Molecular Formula | C48H74O14 |
| Purity | >95% by HPLC |
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Description
Epi-Ivermectin B1a is a degradation product produced by the reversible base-catalyzed isomerization of ivermectin B1a. It is less active than ivermectin against T. urticae (LC90s = 4.0 and 0.038 ppm, respectively).
Specification
| Synonyms | 5-O-demethyl-22,23-dihydro-avermectin A1a; 2-dehydro-4-dihydro Avermectin B1a; epi-dihydro Avermectin B1a; 22,23-dihydro Avermectin B1a; 2-epi-Ivermectin B1a |
| Storage | Store at -20°C under inert atmosphere |
| IUPAC Name | (1S,4S,5'S,6R,6'R,8R,10E,12S,13S,14E,16E,20R,21R,24S)-6'-[(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-5',11,13,22-tetramethylspiro[3,7,19-trioxatetracyclo[15.6.1.14,8.020,24]pentacosa-10,14,16,22-tetraene-6,2'-oxane]-2-one |
| Canonical SMILES | CCC(C)C1C(CCC2(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/C48H74O14/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/h12-15,19,25-26,28,30-31,33-45,49-50,52H,11,16-18,20-24H2,1-10H3/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 | AZSNMRSAGSSBNP-TYECJXEWSA-N |
Properties
| Appearance | Off-white to Light Beige Solid |
| Antibiotic Activity Spectrum | Parasites |
| Boiling Point | 940.4±65.0°C at 760 mmHg |
| Melting Point | 151-160°C |
| Density | 1.2±0.1 g/cm3 |
| Solubility | Slightly soluble in DMSO, Methanol |
Reference Reading
1. Streptomyces avermitilis industrial strain as cell factory for Ivermectin B1a production
Lixin Zhang, Liqiongzi Xiao, Qian Deng, Zixin Deng, Changming Zhao, Yang Liu Synth Syst Biotechnol . 2018 Dec 27;4(1):34-39. doi: 10.1016/j.synbio.2018.12.003.
Ivermectin, a kind of valuable derivatives of Avermectin, is distinct from Avermectin due to the saturated bond at C22-C23 position. Combinatorial biosynthesis of Ivermectins based on Avermectins biosynthetic gene cluster (ave) has been achieved recently, while the establishment of an Ivermectin homogeneous component producing strain is challenging because of the limited compatibility between the native and heterologous polyketide synthase (PKS) domains. In this study, the PKS module 2 Dehydratase (DH)-Enoylreductase (ER)-Ketoreductase (KR) domain set of Meilingmycin, which is another naturally occurring homologue of Avermectin, was employed to substitute the DH-KR domains of Avermectins PKS module 2 to generate an Ivermectin biosynthetic gene cluster (ive). Ivermectins B1a and A1a were heterologously biosynthesized in a classic actinomyces hostStreptomyces lividans. The Avermectin B1a high-producing strainS. avermitilis3-115 was genetically engineered to give an artificial host cell and Ivermectin B1a single component was effectively produced with a production of 1.25 ± 0.14 g/L.
2. B-1a cells protect mice from sepsis-induced acute lung injury
Mian Zhou, Ping Wang, Mahendar Ochani, Thomas L Rothstein, Yasumasa Ode, Nichol E Holodick, Monowar Aziz Mol Med . 2018 May 29;24(1):26. doi: 10.1186/s10020-018-0029-2.
Background:Sepsis morbidity and mortality are aggravated by acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Mouse B-1a cells are a phenotypically and functionally unique sub-population of B cells, providing immediate protection against infection by releasing natural antibodies and immunomodulatory molecules. We hypothesize that B-1a cells ameliorate sepsis-induced ALI.Methods:Sepsis was induced in C57BL/6 mice by cecal ligation and puncture (CLP). PBS or B-1a cells were adoptively transferred into the septic mice intraperitoneally. After 20 h of CLP, lungs were harvested and assessed by PCR and ELISA for pro-inflammatory cytokines (IL-6, IL-1β) and chemokine (MIP-2) expression, by histology for injury, by TUNEL and cleaved caspase-3 for apoptosis, and by myeloperoxidase (MPO) assay for neutrophil infiltration.Results:We found that septic mice adoptively transferred with B-1a cells significantly decreased the mRNA and protein levels of IL-6, IL-1β and MIP-2 in the lungs compared to PBS-treated mice. Mice treated with B-1a cells showed dramatic improvement in lung injury compared to PBS-treated mice after sepsis. We found apoptosis in the lungs was significantly inhibited in B-1a cell injected mice compared to PBS-treated mice after sepsis. B-1a cell treatment significantly down-regulated MPO levels in the lungs compared to PBS-treated mice in sepsis. The protective outcomes of B-1a cells in ALI was further confirmed by using B-1a cell deficient CD19-/-mice, which showed significant increase in the lung injury scores following sepsis as compared to WT mice.Conclusions:Our results demonstrate a novel therapeutic potential of B-1a cells to treat sepsis-induced ALI.
3. Hematopoietic stem cell-independent B-1a lineage
Eliver Eid Bou Ghosn, Yang Yang Ann N Y Acad Sci . 2015 Dec;1362:23-38. doi: 10.1111/nyas.12881.
The accepted dogma has been that a single long-term hematopoietic stem cell (LT-HSC) can reconstitute all components of the immune system. However, our single-cell transfer studies have shown that highly purified LT-HSCs selectively fail to reconstitute B-1a cells in otherwise fully reconstituted hosts (i.e., LT-HSCs fully reconstitute follicular, marginal zone, and B-1b B cells, but not B-1a cells). These results suggest that B-1a cells are a separate B cell lineage that develops independently of classical LT-HSCs. We provide an evolutionary two-pathway development model (HSC independent versus HSC dependent), and suggest that this lineage separation is employed not only by B cells but by all hematopoietic lineages. Collectively, these findings challenge the current notion that LT-HSCs can reconstitute all components of the immune system and raise key questions about human HSC transplantation. We discuss the implications of these findings in light of our recent studies demonstrating the ability of B-1a cells to elicit antigen-specific responses that differ markedly from those mounted by follicular B cells. These findings have implications for vaccine development, in particular vaccines that may elicit the B-1a repertoire.
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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 ╳
