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mmpl3 inhibitors au1235  (MedChemExpress)
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MedChemExpress mmpl3 inhibitors au1235
<t>MmpL3</t> mutations confer resistance to naftifine. Spot dilution assays demonstrate naftifine susceptibility across different M. abscessus strains and complementation constructs. Serial 10-fold dilutions (10 -5 to 10 0 ) of bacterial cultures were spotted onto 7H10-oleic albumin dextrose catalase agar plates containing no drug (0 μg/mL, left), 16 μg/mL naftifine (middle), or 32 μg/mL naftifine (right). ( A ) Wild-type M. abscessus ATCC 19977 (Mab) and strains transformed with vector control, wild-type MmpL3, or mutant MmpL3 alleles (S302T or V299G) show that expression of mutant MmpL3 variants confers naftifine resistance compared to wild-type controls. ( B ) Naftifine-resistant strain Naft R1 (harboring MmpL3 S302T mutation) and its derivatives transformed with vector control or wild-type MmpL3 clones demonstrate that complementation with wild-type MmpL3 does not restore naftifine sensitivity. ( C ) Naftifine-resistant strain Naft R2 (harboring MmpL3 V299G mutation) and its complemented derivatives show that wild-type MmpL3 expression cannot overcome the resistance conferred by the V299G mutation. Colony growth was assessed after 4 days of incubation, indicating that these MmpL3 mutations act dominantly to confer naftifine resistance.
Mmpl3 Inhibitors Au1235, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MmpL3 mutations confer resistance to naftifine. Spot dilution assays demonstrate naftifine susceptibility across different M. abscessus strains and complementation constructs. Serial 10-fold dilutions (10 -5 to 10 0 ) of bacterial cultures were spotted onto 7H10-oleic albumin dextrose catalase agar plates containing no drug (0 μg/mL, left), 16 μg/mL naftifine (middle), or 32 μg/mL naftifine (right). ( A ) Wild-type M. abscessus ATCC 19977 (Mab) and strains transformed with vector control, wild-type MmpL3, or mutant MmpL3 alleles (S302T or V299G) show that expression of mutant MmpL3 variants confers naftifine resistance compared to wild-type controls. ( B ) Naftifine-resistant strain Naft R1 (harboring MmpL3 S302T mutation) and its derivatives transformed with vector control or wild-type MmpL3 clones demonstrate that complementation with wild-type MmpL3 does not restore naftifine sensitivity. ( C ) Naftifine-resistant strain Naft R2 (harboring MmpL3 V299G mutation) and its complemented derivatives show that wild-type MmpL3 expression cannot overcome the resistance conferred by the V299G mutation. Colony growth was assessed after 4 days of incubation, indicating that these MmpL3 mutations act dominantly to confer naftifine resistance.

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: MmpL3 mutations confer resistance to naftifine. Spot dilution assays demonstrate naftifine susceptibility across different M. abscessus strains and complementation constructs. Serial 10-fold dilutions (10 -5 to 10 0 ) of bacterial cultures were spotted onto 7H10-oleic albumin dextrose catalase agar plates containing no drug (0 μg/mL, left), 16 μg/mL naftifine (middle), or 32 μg/mL naftifine (right). ( A ) Wild-type M. abscessus ATCC 19977 (Mab) and strains transformed with vector control, wild-type MmpL3, or mutant MmpL3 alleles (S302T or V299G) show that expression of mutant MmpL3 variants confers naftifine resistance compared to wild-type controls. ( B ) Naftifine-resistant strain Naft R1 (harboring MmpL3 S302T mutation) and its derivatives transformed with vector control or wild-type MmpL3 clones demonstrate that complementation with wild-type MmpL3 does not restore naftifine sensitivity. ( C ) Naftifine-resistant strain Naft R2 (harboring MmpL3 V299G mutation) and its complemented derivatives show that wild-type MmpL3 expression cannot overcome the resistance conferred by the V299G mutation. Colony growth was assessed after 4 days of incubation, indicating that these MmpL3 mutations act dominantly to confer naftifine resistance.

Article Snippet: The MmpL3 inhibitors AU1235, SQ109, and BM212 were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Construct, Transformation Assay, Plasmid Preparation, Control, Mutagenesis, Expressing, Clone Assay, Incubation

Cross-resistance of naftifine-resistant M. abscessus to structurally distinct MmpL3 inhibitors. Dose-response curves show CFU/mL of naftifine-sensitive (Naft S, blue circles) and naftifine-resistant (Naft R1, red squares) M. abscessus strains exposed to serial twofold dilutions (1–128 or 256 μg/mL) of four MmpL3-targeting compounds: naftifine ( A ), BM212 ( B ), AU1235 ( C ), and SQ109 ( D ). Bacterial viability was assessed by CFU enumeration after 3 days of drug treatment, with data points representing mean CFU/mL ± SEM plotted on a logarithmic scale.

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Cross-resistance of naftifine-resistant M. abscessus to structurally distinct MmpL3 inhibitors. Dose-response curves show CFU/mL of naftifine-sensitive (Naft S, blue circles) and naftifine-resistant (Naft R1, red squares) M. abscessus strains exposed to serial twofold dilutions (1–128 or 256 μg/mL) of four MmpL3-targeting compounds: naftifine ( A ), BM212 ( B ), AU1235 ( C ), and SQ109 ( D ). Bacterial viability was assessed by CFU enumeration after 3 days of drug treatment, with data points representing mean CFU/mL ± SEM plotted on a logarithmic scale.

Article Snippet: The MmpL3 inhibitors AU1235, SQ109, and BM212 were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: