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Details

Stereochemistry ACHIRAL
Molecular Formula C21H23F2N3O4
Molecular Weight 419.4218
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 1
Charge 0

SHOW SMILES / InChI
Structure of ACORAFLOXACIN

SMILES

COC1=C(N2CCC\C(C2)=C(/F)CN)C(F)=CC3=C1N(C=C(C(O)=O)C3=O)C4CC4

InChI

InChIKey=VMKVDAAFMQKZJS-LFIBNONCSA-N
InChI=1S/C21H23F2N3O4/c1-30-20-17-13(19(27)14(21(28)29)10-26(17)12-4-5-12)7-15(22)18(20)25-6-2-3-11(9-25)16(23)8-24/h7,10,12H,2-6,8-9,24H2,1H3,(H,28,29)/b16-11+

HIDE SMILES / InChI

Molecular Formula C21H23F2N3O4
Molecular Weight 419.4218
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 1
Optical Activity NONE

Description

Acorafloxacin (JNJ-Q2) is a fluoroquinolone that was developed by Furiex Pharmaceuticals (a subsidiary of Forest Laboratories) for the treatment of complicated skin and and soft tissue infections. Acorafloxacin was originally developed by Janssen, then licensed to Furiex Pharmaceuticals (now a part of Actavis). JNJ-Q2 has excellent in vitro and in vivo activity against a variety of Gram-positive and Gram-negative organisms. In vitro studies indicate that JNJ-Q2 has potent activity against pathogens responsible for acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP), such as Staphylococcus aureus and Streptococcus pneumoniae. JNJ-Q2 also has been shown to have a higher barrier to resistance compared to other agents in the class and it remains highly active against drug-resistant organisms, including methicillin-resistant S. aureus, ciprofloxacin-resistant methicillin-resistant S. aureus, and drug-resistant S. pneumoniae. In two Phase II studies, the efficacy of JNJ-Q2 was comparable to linezolid for ABSSSI and moxifloxacin for CABP. Furthermore, JNJ-Q2 was well tolerated, with adverse event rates similar to or less than other fluoroquinolones. Acorafloxacin inhibits MuRF enzyme, required for cell wall synthesis. Acorafloxacin directly inhibits bacterial DNA synthesis by halting the activity of DNA gyrase (responsible for negative helical supercoiling) and DNA topoisomerase IV (responsible for separating the nucleotide strands). Fast track designation and qualified infectious disease product designation (QIDP) was granted by FDA for the treatment of bacterial infections in 2013.

Originator

Approval Year

PubMed

Patents

Sample Use Guides

In Vivo Use Guide
A double-blind, multicenter, phase II noninferiority study treated 161 patients for 7 to 14 days, testing the efficacy of JNJ-Q2 (250 mg, twice a day [BID]) versus linezolid (600 mg, BID) in patients with acute bacterial skin and skin structure infections (ABSSSI).
Route of Administration: Oral
In Vitro Use Guide
Against a set of 118 recent clinical isolates of Streptococcus pneumoniae, including fluoroquinolone-resistant variants bearing multiple DNA topoisomerase target mutations, an MIC(90) value for JNJ-Q2 of 0.12 ug/ml was determined, indicating that it was 32-fold more potent than moxifloxacin. Against a collection of 345 recently collected methicillin-resistant Staphylococcus aureus (MRSA) isolates, including 256 ciprofloxacin-resistant strains, the JNJ-Q2 MIC(90) value was 0.25 ug/ml, similarly indicating that it was 32-fold more potent than moxifloxacin.
Substance Class Chemical
Record UNII
070SV15RJA
Record Status Validated (UNII)
Record Version