Details
Stereochemistry | ACHIRAL |
Molecular Formula | C7H7NO3.C6H7N3O |
Molecular Weight | 290.2747 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
NNC(=O)C1=CC=NC=C1.NC2=CC=C(C(O)=O)C(O)=C2
InChI
InChIKey=RKPHTRVPGYGVQD-UHFFFAOYSA-N
InChI=1S/C7H7NO3.C6H7N3O/c8-4-1-2-5(7(10)11)6(9)3-4;7-9-6(10)5-1-3-8-4-2-5/h1-3,9H,8H2,(H,10,11);1-4H,7H2,(H,9,10)
DescriptionSources: https://www.ncbi.nlm.nih.gov/pubmed/13335882Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/13595397 | https://www.drugs.com/international/pasiniazid.html | https://www.ncbi.nlm.nih.gov/pubmed/28131606 | https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1553312b-ed76-421c-a055-2579bdcf366c#i4i_indications_id_indications | http://www.drugbank.ca/drugs/DB00233 | https://www.ncbi.nlm.nih.gov/pubmed/15151838
Sources: https://www.ncbi.nlm.nih.gov/pubmed/13335882
Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/13595397 | https://www.drugs.com/international/pasiniazid.html | https://www.ncbi.nlm.nih.gov/pubmed/28131606 | https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1553312b-ed76-421c-a055-2579bdcf366c#i4i_indications_id_indications | http://www.drugbank.ca/drugs/DB00233 | https://www.ncbi.nlm.nih.gov/pubmed/15151838
Pasiniazid is a composition of isoniazid and 4-aminosalicylic acid, that has mutual effects coupling isoniazid and 4-aminosalicylic acid for use in tuberculosis patients. Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically M. tuberculosis, M. bovis and M. kansasii. Isoniazid is a prodrug and must be activated by bacterial catalase. Isoniazid inhibits InhA, the enoyl reductase from Mycobacterium tuberculosis, by forming a covalent adduct with the NAD cofactor. 4-Aminosalicylic acid is an anti-tuberculosis drug used to treat tuberculosis in combination with other active agents. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in the folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slow. Secondly, the aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL1849 Sources: http://www.ncbi.nlm.nih.gov/pubmed/14623976 |
0.75 µM [Ki] | ||
Target ID: CHEMBL6065 Sources: https://www.ncbi.nlm.nih.gov/pubmed/23779105 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Curative | Jieheqing Approved UseUnknown |
Sample Use Guides
A single oral dose of 1200 mg pasiniazide and dipasic tablets was given according to a cross over design.
Route of Administration:
Oral
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/28131606
Minimum inhibitory concentration (MIC) determination. Inocula were prepared from actively growing bacteria collected from LJ slants or Middlebrook 7H10 agar plates. Inocula were adjusted with saline to a cell density of 1.5 x 10^8 cells/mL (0.5 McFarland standard) and were then diluted (1:200) using CA-MHB for RGM or CAMHB+ 5% ADC supplement (CA-MHB-S) for SGM. Dipasic (Pasiniazid) were serially diluted two-fold in 100 μL of CA-MHB or CA-MHB-S. The final reaction volume was 200 μL (100 μL of the antibiotic solution and 100 μL of the bacterial suspension). Three negative controls were used as part of this study: medium without antibiotics was used to determine the addition time for alamarBlue; Medium without inoculum was used to determine the interference to alamarBlue by the medium; and a series of concentration gradients for Dipasic were used to determine the interference to alamarBlue by the drug–medium mixture colour. The plates were sealed in individual Ziploc bags and were incubated at 37 °C. After 24 h for RGM or 6 days for SGM, the first drug-free growth control wells were examined using an indicator (20 μL of alamarBlue and 50 μL of sterile 5% Tween-80). The plateswere then re-incubated for 24 h. If the control well changed to a pink colour, all of the wells containing drugs were supplemented with the indicator. After a further 24 h of incubation, the colour of all of the wells was recorded. Each MIC for the tested drug was recorded on a daily basis between the third and sixth days for RGM and between the seventh and eleventh days for SGM. The MIC was defined as the lowest drug concentration that prevented a change in colour.
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m6502
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C008767
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218-183-2
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SUB09635MIG
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PARENT (SALT/SOLVATE)
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