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Fig. 1 · Structure
Cat. No.
A10791
CAS No.
13292-46-1
Formula
C43H58N4O12
Mol. Weight
822.9

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Rifampin

Cat. No. A10791 CAS 13292-46-1

RNA polymerase inhibitor

Antibiotic; inhibits bacterial RNA polymerase. Prototypical activator of the pregnane X receptor (PXR).

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Publications for Rifampin

1 publication citing this product

  1. Meikle V, .et al. , Antimicrob Agents Chemother, 2018, Nov 12. pii: AAC.01846-18 PMID: 30420480
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Biological Activity

Bioactivity / Mechanism

Rifampicin inhibited purified bacterial RNA polymerase in a mechanistic study without measurably reducing active-center Fe2+ or Mg2+ binding affinity. Transcription was reported as completely inhibited at 1.2 μM in the accompanying control. These results argue against reduced Mg2+ affinity as the explanation for inhibition in this assay. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
RNA polymerase

Cellular Effect

Cell Line Activity Value Description Reference
A549 GI50 > 100 μg/mL Cytotoxicity against human A549 cells incubated for 1 to 11 days by MTT assay 10.1039/C5MD00404G
A549 GI50 > 100 μg/mL Cytotoxicity against human A549 cells assessed as growth inhibition after 48 hrs by MTT assay [PMID: 28110868]
A549 GI50 > 100 μg/mL Cytotoxicity against human A549 cells after 48 hrs by MTT assay [PMID: 27013391]
A549 GI50 > 100 μg/mL Growth inhibition of human A549 cells by MTT assay [PMID: 30910461]
A549 GI50 > 100 μg/mL Growth inhibition of human A549 cells by MTT assay [PMID: 28411559]
A549 GI50 > 121.51 mM Cytotoxicity against human A549 cells by MTT assay 10.1039/C6MD00278A
B-cell IC50 96 μM Antiproliferative activity against Theileria parva-induced proliferation of bovine B lymphocyte assessed as inhibition of [3H]thymidine uptake after 48 hrs [PMID: 19075064]
CHO CC50 512 μM Cytotoxicity against CHO cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 31525660]
HCT-116 GI50 > 100 μg/mL Cytotoxicity against human HCT116 cells incubated for 1 to 11 days by MTT assay 10.1039/C5MD00404G
HCT-116 GI50 > 100 μg/mL Cytotoxicity against human HCT116 cells assessed as growth inhibition after 48 hrs by MTT assay [PMID: 28110868]
HCT-116 GI50 > 100 μg/mL Cytotoxicity against human HCT116 cells by MTT assay [PMID: 27914801]
HCT-116 CC50 > 100 μg/mL Cytotoxicity against human HCT116 cells by MTT assay [PMID: 27301367]
HCT-116 GI50 > 121.51 mM Cytotoxicity against human HCT116 cells by MTT assay 10.1039/C6MD00278A
HEK293 CC50 > 100 μM Cytotoxicity against HEK293 cells assessed as reduction in cell viability after 48 hrs by Alamar Blue reporter assay [PMID: 30392371]
HEK293 IC50 0.3 μM Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estradiol-17beta-glucuronide substrate [PMID: 22587986]
HEK293 EC50 1.1 μM Agonist activity at human PXR transfected in HEK293 cells after 24 hrs by luciferase reporter gene assay [PMID: 26905831]
HEK293 IC50 1.2 μM Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake by scintillation counting [PMID: 22541068]
HEK293 IC50 1.5 μM Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake incubated for 5 mins by scintillation counting [PMID: 22541068]
HEK293 IC50 2.2 μM Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using pitavastatin substrate [PMID: 22587986]
HEK293 IC50 2.3 μM Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estrone-3-sulfate substrate [PMID: 22587986]

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In Vitro Studies

In primary human hepatocytes from six donors, 24 h rifampin exposure induced CYP3A4 and ABCB1 mRNA. At 10 μM, the authors reported 80-fold and 5-fold induction, respectively (P = 0.03 for each). Responses varied between donors, and mRNA induction does not establish a corresponding change in enzyme or transporter activity. [2]

RNAP inhibition without reduced active-center metal-ion affinity

Biochemical assay · Purified bacterial RNAP holoenzyme and RNAP–promoter open complexes (RPο) [1]

Rifampicin inhibited transcription while active-center Fe2+ and Mg2+ binding remained indistinguishable from no-rifampicin controls within experimental error. Concentration-response controls verified inhibition at the rifampicin concentration used for the binding comparisons. This tests the proposed Mg2+-affinity mechanism; it does not by itself map the steric binding site.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Active-center Fe2+ and Mg2+ binding with versus without rifampicinComparative binding affinity Indistinguishable within experimental error[1]
Transcription control for saturation in binding experimentsTranscription inhibition Completely inhibited at 1.2 μM rifampicin (reported in Results)[1]

Literature-Reported Treatment Conditions

Treatment concentration
1.2 μM rifampicin for binding comparisons; concentration-response inhibition control shown in Figure 1C
Method
Cell-free RNAP assays with paired no-rifampicin controls; tagged RNAP cleavage assay described in main Methods.
Co-treatment
No second antibacterial drug; Fe2+ probe and competing Mg2+ are assay components.
Reported limits
Detailed SI methods were not retrieved; incubation duration, solvent and preparation details are not supplied here. Main text and Figure 1 establish the named material, comparison and saturation control.
Methods and source locations

Compound reported in the paper: Rifampicin; Compound label in the paper: rifampicin

Named-compound biochemical evidence only; no A10791 lot equivalence, pathogen growth protocol or resistance-selection claim.

Results: Absence of Effects of Rifamycins on Metal-Ion Binding; Figure 1A–C and caption; main Methods: Fe2+-Mediated Cleavage Experiments

Active-center Fe2+ and Mg2+ binding with versus without rifampicin: Fe2+-mediated cleavage of the β′ NADFDGD motif; competing Mg2+ used to infer Mg2+ affinity. — Results: Absence of Effects of Rifamycins on Metal-Ion Binding; Figure 1A–C and caption; main Methods: Fe2+-Mediated Cleavage Experiments

Transcription control for saturation in binding experiments: Transcription measured across rifampicin concentrations alongside metal-binding readouts; no potency estimate inferred from the curve. — Figure 1C and accompanying Results paragraph

Rifampin-induced gene expression in primary human hepatocytes

Cell-based study · Cryopreserved primary human hepatocytes from 6 donors; experiments completed in triplicate [2]

Rifampin induced CYP3A4 and ABCB1 mRNA in a concentration-dependent manner. The authors reported the greatest induction at 10 μM: 80-fold for CYP3A4 and 5-fold for ABCB1 (P = 0.03 for each). Donor variability was substantial; these endpoints do not establish enzyme or transporter activity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
CYP3A4 mRNA at 10 μM rifampin versus matched 0 μM controlFold induction 80-fold; P = 0.03[2]
ABCB1 mRNA at 10 μM rifampin versus matched 0 μM controlFold induction 5-fold; P = 0.03[2]

Literature-Reported Treatment Conditions

Treatment concentration
0.5, 5, and 10 μM; 0 μM matched control
Exposure duration
24 h
Method
Separate rifampin exposure of primary human hepatocytes followed by RNA extraction, reverse transcription and real-time PCR.
Vehicle
10 mM stock in methanol diluted in hepatocyte medium; control contained the same volume of methanol and medium.
Co-treatment
None; rifabutin and rifapentine were separate comparator exposures, not co-treatments.
Reported limits
Final methanol percentage and lot-specific purity/stereochemical analysis were not reported in the main report.
Methods and source locations

Compound reported in the paper: Rifampin; Compound label in the paper: RIF

Human-cell transcriptional response; no human treatment recommendation or direct functional drug-interaction magnitude.

Main report: material preparation, hepatocyte treatment and qPCR methods; Figure 1 and caption; Results paragraph beginning “Rifampin elicited”; discussion of interdonor variation and mRNA/activity limits

CYP3A4 mRNA at 10 μM rifampin versus matched 0 μM control: Real-time PCR normalized to GAPDH and matched control by comparative CT (2^−ΔΔCT); 6 donors completed in triplicate. — Main report: material preparation, hepatocyte treatment and qPCR methods; Figure 1 and caption; Results paragraph beginning “Rifampin elicited”; discussion of interdonor variation and mRNA/activity limits

ABCB1 mRNA at 10 μM rifampin versus matched 0 μM control: Same qPCR design and normalization. Reported values taken from Results text rather than estimated from box plots. — Main report: material preparation, hepatocyte treatment and qPCR methods; Figure 1 and caption; Results paragraph beginning “Rifampin elicited”; discussion of interdonor variation and mRNA/activity limits

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 13292-46-1
Applications RNA polymerase inhibitor
Formula C43H58N4O12
Molecular Weight 822.9
Synonyms Rifampicin
SMILES
C[C@H]1/C=C/C=C(\C(=O)NC\2=C(C3=C(C(=C4C(=C3C(=O)/C2=C/NN5CCN(CC5)C)C(=O)[C@](O4)(O/C=C/[C@@H]([C@H]([C@H]([C@@H]([C@@H]([C@@H]([C@H]1O)C)O)C)OC(=O)C)C)OC)C)C)O)O)/C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 94 mg/mL (114.22 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Feklistov A, Mekler V, Jiang Q, et al. Rifamycins do not function by allosteric modulation of binding of Mg2+ to the RNA polymerase active center. Proceedings of the National Academy of Sciences of the United States of America (2008). PMID: 18787125 DOI: 10.1073/pnas.0802822105 Source material
  2. [2] Williamson B, Dooley KE, Zhang Y, et al. Induction of influx and efflux transporters and cytochrome P450 3A4 in primary human hepatocytes by rifampin, rifabutin, and rifapentine. Antimicrobial agents and chemotherapy (2013). PMID: 24060875 DOI: 10.1128/aac.01124-13 Source material

Publications

1 publication citing this product

  1. Meikle V, .et al. , Antimicrob Agents Chemother, 2018, Nov 12. pii: AAC.01846-18 PMID: 30420480

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