CAS NO: | 13292-46-1 |
规格: | ≥98% |
包装 | 价格(元) |
500mg | 电议 |
1g | 电议 |
2g | 电议 |
5g | 电议 |
10g | 电议 |
50g | 电议 |
Molecular Weight (MW) | 822.94 |
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Formula | C43H58N4O12 |
CAS No. | 13292-46-1 (Rifampicin); |
Storage | -20℃ for 3 years in powder form |
-80℃ for 2 years in solvent | |
Solubility (In vitro) | DMSO: 100 mg/mL (121.5 mM) |
Water: <1 mg/mL | |
Ethanol: <1 mg/mL | |
Other info | Chemical Name: (7S,9E,11S,12R,13S,14R,15R,16R,17S,18S,19E,21Z)-2,15,17,27,29-pentahydroxy-11-methoxy-3,7,12,14,16,18,22-heptamethyl-26-{(E)-[(4-methylpiperazin-1-yl)imino]methyl}-6,23-dioxo-8,30-dioxa-24-azatetracyclo[23.3.1.1(4,7).0(5,28)]triaconta-1(28),2,4,9,19,21,25(29),26-octaen-13-yl acetate InChi Key: JQXXHWHPUNPDRT-WLSIYKJHSA-N InChi Code: InChI=1S/C43H58N4O12/c1-21-12-11-13-22(2)42(55)45-33-28(20-44-47-17-15-46(9)16-18-47)37(52)30-31(38(33)53)36(51)26(6)40-32(30)41(54)43(8,59-40)57-19-14-29(56-10)23(3)39(58-27(7)48)25(5)35(50)24(4)34(21)49/h11-14,19-21,23-25,29,34-35,39,49-53H,15-18H2,1-10H3,(H,45,55)/b12-11+,19-14+,22-13-,44-20+/t21-,23+,24+,25+,29-,34-,35+,39+,43-/m0/s1 SMILES Code: CC(O[C@@H]([C@H](C)[C@H](O)[C@H](C)[C@@H](O)[C@@H](C)/C=C/C=C(C)\C(N1)=O)[C@H](C)[C@@H](OC)/C=C/O[C@](O2)(C)C(C3=C2C(C)=C(O)C4=C3C(O)=C(/C=N/N5CCN(C)CC5)C1=C4O)=O)=O |
Synonyms | Rimactane; Arficin; Arzide; Rifampicin; Rifadin; Rifampin; Rimactane; Rimactan; Tubocin; Archidyn; Benemicin; Doloresum; Eremfat; Fenampicin; Sinerdol; |
In Vitro | In vitro activity: Rifampin inhibits IκBα degradation and mitogen-activated protein kinase (MAPK) phosphorylation. Rifampin is found to bind to human MD-2 in a Rifampin and MD-2 concentration-dependent manner. Rifampin inhibits NF-κB activation induced by LPS (20 ng/ml) in a dose-dependent manner, with an IC50 of 44.1 μM in Blue hTLR4 293 cells (A) and immunocompetent microgial BV-2 cell. Rifampin (50 μM) suppresses NF-κB activation at varying LPS doses, and the maximum NF-κB level induced by LPS in the presence of Rifampin (50 μM) is much lower than that in the absence of Rifampin. Rifampin inhibits NO production induced by LPS (200 ng/ml) in a dose-dependent manner in BV-2 cells, with an IC50 of 21.2 μM. Rifampin suppresses LPS induced TNF-α and IL-1β production in both microglia BV-2 and RAW 264.7 macrophage cells. Rifampin-inhibiting innate immune signaling is independent of the pregnane X receptor NR1I2. Rifampin combined with polyester vascular prostheses (PVP) functionalised with cyclodextrin (PVP-CD) results in significant bacterial adhesion reduction and growth inhibition against Gram-positive bacteria. Rifampin (50 μg/mL) significantly reduces the CFU counts of stationary-phase cultures and reduces the CFU counts of the log-phase culture to zero. Rifampin is particularly suitable since it is bactericidal and starts killing M. tuberculosis within an hour of exposure. |
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In Vivo | Rifampicin (200, 400 mg/kg) can induce fatty liver at high concentration. Rifampicin (30 mg/kg, i.p.) treatment of S464P biofilms in vivo results in a slight decline, but earlier rebinds in bioluminescence from these catheters compared with the parental signal, whereas rifampicin has no affect on bioluminescence in mice infected with mutant H481Y. |
Animal model | Mice |
Formulation & Dosage | 30 mg/kg, i.p.; Briefly, 1 cm Teflon catheter (14-gauge) carrying 104 cfu S. aureus, either the parental strain Xen 29 or the RifR mutants S464P or H481Y, are implanted subcutaneously in groups of nine mice per strain. One catheter segment is inserted on each side of each animal. Six days after the implantation of the catheters, five mice from each group are treated with rifampicin at 30 mg/kg intraperitoneally in 0.1 mL saline, twice daily for four consecutive days. The remaining four mice in each group are left untreated as controls. At various time points during the infection, the mice are anaesthetized using a constant flow of 1.5% isoflurane from the IVIS(R) manifold, and imaged using an IVIS(R) Image System 100 Series. The bioluminescent signals (photons/s) emitted from the mice are analysed using LivingImage(R) software and plotted over the course of infection. The mice are sacrificed 20 days after infection (11 days after final rifampicin treatment). The catheters are surgically removed and the bacteria are detached by sonication for determination of bacterial burdens on the catheters. |
References | FASEB J. 2013 Jul;27(7):2713-22; J Infect. 2014 Feb;68(2):116-24. |