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ATCC reference strain m abscessus atcc 19977 t

Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) <t>ATCC</t> <t>19977</t> <t>T</t> smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Reference Strain M Abscessus Atcc 19977 T, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1249 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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reference strain m abscessus atcc 19977 t - by Bioz Stars, 2026-09

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1) Product Images from "Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection"

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

Journal: Antimicrobial Agents and Chemotherapy

doi: 10.1128/aac.01105-25

Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Figure Legend Snippet: Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Techniques Used: Concentration Assay, Infection, Variant Assay, Control

Dose-dependent cytotoxicity analysis in uninfected and M. abscessus -infected cells. ( A ) Representative flow cytometry dot plots show Annexin V and 7-AAD staining patterns in uninfected (UI) and infected (IN) cells treated with increasing concentrations (0, 10, 30, and 90 μM) of the test compound. THP-1 cells were infected with M. abscessus ATCC 19977 T smooth variants and treated with naftifine for 3 days. Gated regions indicate dead cells (Annexin V + , including early and late apoptotic and necrotic populations). ( B and C ) Quantification of cell death shows the percentage of Annexin V + population (both 7-AAD + and 7-AAD⁻) in uninfected ( B ) and infected ( C ) cells. Data represent mean ± SEM from at least three independent experiments. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons against the control. ** P < 0.01 and **** P < 0.0001 compared to untreated control (0 μM).

Figure Legend Snippet: Dose-dependent cytotoxicity analysis in uninfected and M. abscessus -infected cells. ( A ) Representative flow cytometry dot plots show Annexin V and 7-AAD staining patterns in uninfected (UI) and infected (IN) cells treated with increasing concentrations (0, 10, 30, and 90 μM) of the test compound. THP-1 cells were infected with M. abscessus ATCC 19977 T smooth variants and treated with naftifine for 3 days. Gated regions indicate dead cells (Annexin V + , including early and late apoptotic and necrotic populations). ( B and C ) Quantification of cell death shows the percentage of Annexin V + population (both 7-AAD + and 7-AAD⁻) in uninfected ( B ) and infected ( C ) cells. Data represent mean ± SEM from at least three independent experiments. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons against the control. ** P < 0.01 and **** P < 0.0001 compared to untreated control (0 μM).

Techniques Used: Infection, Flow Cytometry, Staining, Control

Naftifine exhibits bacteriostatic activity against M. abscessus in axenic culture. Time-kill assays were performed to evaluate the antimicrobial activity of naftifine against different M. abscessus strains and morphological variants. ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Bacterial cultures in logarithmic growth phase were treated with naftifine at concentrations ranging from 2 to 64 µg/mL (equivalent to 6–198 μM) or DMSO vehicle control. Samples were collected at 24-hour intervals over a 96-hour incubation period, and bacterial viability was assessed by CFU enumeration following serial dilution plating. Data represent mean ± SEM from two independent experiments performed in triplicate. Statistical comparisons between naftifine-treated and DMSO control at each time point were performed using two-way ANOVA with Tukey’s multiple comparisons test. Statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Figure Legend Snippet: Naftifine exhibits bacteriostatic activity against M. abscessus in axenic culture. Time-kill assays were performed to evaluate the antimicrobial activity of naftifine against different M. abscessus strains and morphological variants. ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Bacterial cultures in logarithmic growth phase were treated with naftifine at concentrations ranging from 2 to 64 µg/mL (equivalent to 6–198 μM) or DMSO vehicle control. Samples were collected at 24-hour intervals over a 96-hour incubation period, and bacterial viability was assessed by CFU enumeration following serial dilution plating. Data represent mean ± SEM from two independent experiments performed in triplicate. Statistical comparisons between naftifine-treated and DMSO control at each time point were performed using two-way ANOVA with Tukey’s multiple comparisons test. Statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Techniques Used: Activity Assay, Variant Assay, Control, Incubation, Serial Dilution

Naftifine reduces M. abscessus burden in the lungs and spleens of immunosuppressed mice. BALB/c mice were immunosuppressed with dexamethasone and subsequently infected intranasally with 1,000 CFU of M. abscessus ATCC 19977 T rough variant. Treatment began 3 days post-infection and continued once daily for 14 days. Mice received either naftifine HCl (50 mg/kg of body weight, intraperitoneal), cefoxitin (200 mg/kg of body weight, subcutaneous, positive control), or PBS vehicle control (intraperitoneal). After the treatment period, mice were euthanized, and bacterial loads in the ( A ) lungs and ( B ) spleens were quantified by CFU enumeration and expressed as log 10 CFU per organ. Data represent individual mice with mean ± SEM. ( C ) Representative hematoxylin and eosin-stained lung sections from infected mice treated with PBS vehicle control (top panels) or naftifine (bottom panels) are shown at 4×, 10×, and 40× magnifications to illustrate histopathological changes. Statistical comparisons between treatment groups were performed with the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. * P < 0.05; ** P < 0.01; *** P < 0.001 and ns, not significant.

Figure Legend Snippet: Naftifine reduces M. abscessus burden in the lungs and spleens of immunosuppressed mice. BALB/c mice were immunosuppressed with dexamethasone and subsequently infected intranasally with 1,000 CFU of M. abscessus ATCC 19977 T rough variant. Treatment began 3 days post-infection and continued once daily for 14 days. Mice received either naftifine HCl (50 mg/kg of body weight, intraperitoneal), cefoxitin (200 mg/kg of body weight, subcutaneous, positive control), or PBS vehicle control (intraperitoneal). After the treatment period, mice were euthanized, and bacterial loads in the ( A ) lungs and ( B ) spleens were quantified by CFU enumeration and expressed as log 10 CFU per organ. Data represent individual mice with mean ± SEM. ( C ) Representative hematoxylin and eosin-stained lung sections from infected mice treated with PBS vehicle control (top panels) or naftifine (bottom panels) are shown at 4×, 10×, and 40× magnifications to illustrate histopathological changes. Statistical comparisons between treatment groups were performed with the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. * P < 0.05; ** P < 0.01; *** P < 0.001 and ns, not significant.

Techniques Used: Infection, Variant Assay, Positive Control, Control, Staining

Autophagy contributes to the intracellular efficacy of naftifine against M. abscessus . Intracellular bacterial survival (log 10 CFU) of ( A ) naftifine-sensitive M. abscessus ATCC 19977 T S (Mab S, blue) strain and naftifine-resistant M. abscessus strain (Mab-Naft R1, red) in wild-type RAW 264.7 macrophages (filled circles) or ( B ) ATG16L1 knockdown macrophages (open circles) treated with naftifine at 0, 5, 10, and 20 µM. Bacterial loads were quantified on days 1 (D1) and 2 (D2) post-infection. ( C and D ) Representative immunoblots showing LC3-I/LC3-II expression and β-actin (loading control) in macrophage lysates at day 1 post-infection with ( C ) Mab-Naft S or ( D ) Mab-Naft R1, treated with indicated naftifine concentrations (μM). Data represent mean ± SEM. Statistical significance was determined by two-way ANOVA. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Figure Legend Snippet: Autophagy contributes to the intracellular efficacy of naftifine against M. abscessus . Intracellular bacterial survival (log 10 CFU) of ( A ) naftifine-sensitive M. abscessus ATCC 19977 T S (Mab S, blue) strain and naftifine-resistant M. abscessus strain (Mab-Naft R1, red) in wild-type RAW 264.7 macrophages (filled circles) or ( B ) ATG16L1 knockdown macrophages (open circles) treated with naftifine at 0, 5, 10, and 20 µM. Bacterial loads were quantified on days 1 (D1) and 2 (D2) post-infection. ( C and D ) Representative immunoblots showing LC3-I/LC3-II expression and β-actin (loading control) in macrophage lysates at day 1 post-infection with ( C ) Mab-Naft S or ( D ) Mab-Naft R1, treated with indicated naftifine concentrations (μM). Data represent mean ± SEM. Statistical significance was determined by two-way ANOVA. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Techniques Used: Knockdown, Infection, Western Blot, Expressing, Control

Synergistic interactions between naftifine and β-lactam antibiotics against M. abscessus . Checkerboard assays were performed to evaluate drug interactions between naftifine ( y -axis) and various antibiotics ( x -axis) against M. abscessus ATCC 19977 T smooth variant. Heat maps display the percentage of bacterial growth, with darker blue indicating greater growth. Twofold serial dilutions of each drug were tested in combination, and growth inhibition was assessed after incubation. Naftifine showed indifferent interactions with clarithromycin ( A ) and tigecycline ( E ), additive/partial synergistic effects with amikacin ( B ), but demonstrated synergistic effects when combined with the β-lactam antibiotics cefoxitin ( C ) and imipenem ( D ), particularly at sub-inhibitory concentrations. Synergy was defined as FICI ≤ 0.5, where the combined effect significantly exceeded the sum of individual drug activities. Data were analyzed and plotted using GraphPad Prism version 10.

Figure Legend Snippet: Synergistic interactions between naftifine and β-lactam antibiotics against M. abscessus . Checkerboard assays were performed to evaluate drug interactions between naftifine ( y -axis) and various antibiotics ( x -axis) against M. abscessus ATCC 19977 T smooth variant. Heat maps display the percentage of bacterial growth, with darker blue indicating greater growth. Twofold serial dilutions of each drug were tested in combination, and growth inhibition was assessed after incubation. Naftifine showed indifferent interactions with clarithromycin ( A ) and tigecycline ( E ), additive/partial synergistic effects with amikacin ( B ), but demonstrated synergistic effects when combined with the β-lactam antibiotics cefoxitin ( C ) and imipenem ( D ), particularly at sub-inhibitory concentrations. Synergy was defined as FICI ≤ 0.5, where the combined effect significantly exceeded the sum of individual drug activities. Data were analyzed and plotted using GraphPad Prism version 10.

Techniques Used: Variant Assay, Inhibition, Incubation

Infection:

Article Title: Efficacy of regimens targeting Mycobacterium abscessus in vitro and in vivo
Article Snippet: .. Subsequently, mice were intravenously infected via the tail vein with M. abscessus reference strain ATCC 19977 at a dose of 2 × 106 CFU per mouse. ..

Article Title: TBAJ-587, a novel diarylquinoline, is active against Mycobacterium abscessus
Article Snippet: .. Shanghai, China), were infected with M. abscessus reference strain ATCC 19977, M. massiliense reference strain CIP 108297, and clinical isolates M. abscessus G103 (subsp. abscessus ) or G105 (subsp. massiliense ) at a multiplicity of infection = 10 as described previously ( ). .. Cell lysates, prepared 4, 24, 48, and 72 hours after the addition of TBAJ-587 or BDQ, were spread onto Middlebrook 7H10 agar plates supplemented with 10% OADC enrichment.

Variant Assay:

Article Title: Novel Synergies and Isolate Specificities in the Drug Interaction Landscape of Mycobacterium abscessus
Article Snippet: .. To generate a systematic data set of drug interaction profiles comparable to other published drug interaction studies, we measured drug pair responses in the M. abscessus reference strain ATCC 19977, a Mycobacterium abscessus subsp. abscessus variant that harbors erm (41) (erythromycin ribosomal methylase gene), whose presence is associated with inducible macrolide resistance ( , ). ..

Article Title: Novel Synergies and Isolate Specificities in the Drug Interaction Landscape of Mycobacterium abscessus.
Article Snippet: Design of systematic drug interaction study in ATCC 19977. .. To generate a systematic data set of drug interaction profiles comparable to other published drug interaction studies, we measured drug pair responses in the M. abscessus reference strain ATCC 19977, a Mycobacterium abscessus subsp. abscessus variant that harbors erm(41) (erythromycin ribosomal methylase gene), whose presence is associated with inducible macrolide resistance (9, 10). ..

other:

Article Title: Predicting Mycobacterium abscessus proteins with atypical amino acid composition essential for human infections
Article Snippet: To identify these proteins, we used the annotated genome of the M. abscessus reference strain ATCC 19977, which belongs to the subspecies abscessus , the most commonly seen in clinical infections ( ).

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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: Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Concentration Assay, Infection, Variant Assay, Control

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: Dose-dependent cytotoxicity analysis in uninfected and M. abscessus -infected cells. ( A ) Representative flow cytometry dot plots show Annexin V and 7-AAD staining patterns in uninfected (UI) and infected (IN) cells treated with increasing concentrations (0, 10, 30, and 90 μM) of the test compound. THP-1 cells were infected with M. abscessus ATCC 19977 T smooth variants and treated with naftifine for 3 days. Gated regions indicate dead cells (Annexin V + , including early and late apoptotic and necrotic populations). ( B and C ) Quantification of cell death shows the percentage of Annexin V + population (both 7-AAD + and 7-AAD⁻) in uninfected ( B ) and infected ( C ) cells. Data represent mean ± SEM from at least three independent experiments. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons against the control. ** P < 0.01 and **** P < 0.0001 compared to untreated control (0 μM).

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Flow Cytometry, Staining, Control

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: Naftifine exhibits bacteriostatic activity against M. abscessus in axenic culture. Time-kill assays were performed to evaluate the antimicrobial activity of naftifine against different M. abscessus strains and morphological variants. ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Bacterial cultures in logarithmic growth phase were treated with naftifine at concentrations ranging from 2 to 64 µg/mL (equivalent to 6–198 μM) or DMSO vehicle control. Samples were collected at 24-hour intervals over a 96-hour incubation period, and bacterial viability was assessed by CFU enumeration following serial dilution plating. Data represent mean ± SEM from two independent experiments performed in triplicate. Statistical comparisons between naftifine-treated and DMSO control at each time point were performed using two-way ANOVA with Tukey’s multiple comparisons test. Statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Activity Assay, Variant Assay, Control, Incubation, Serial Dilution

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: Naftifine reduces M. abscessus burden in the lungs and spleens of immunosuppressed mice. BALB/c mice were immunosuppressed with dexamethasone and subsequently infected intranasally with 1,000 CFU of M. abscessus ATCC 19977 T rough variant. Treatment began 3 days post-infection and continued once daily for 14 days. Mice received either naftifine HCl (50 mg/kg of body weight, intraperitoneal), cefoxitin (200 mg/kg of body weight, subcutaneous, positive control), or PBS vehicle control (intraperitoneal). After the treatment period, mice were euthanized, and bacterial loads in the ( A ) lungs and ( B ) spleens were quantified by CFU enumeration and expressed as log 10 CFU per organ. Data represent individual mice with mean ± SEM. ( C ) Representative hematoxylin and eosin-stained lung sections from infected mice treated with PBS vehicle control (top panels) or naftifine (bottom panels) are shown at 4×, 10×, and 40× magnifications to illustrate histopathological changes. Statistical comparisons between treatment groups were performed with the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. * P < 0.05; ** P < 0.01; *** P < 0.001 and ns, not significant.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Variant Assay, Positive Control, Control, Staining

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: Autophagy contributes to the intracellular efficacy of naftifine against M. abscessus . Intracellular bacterial survival (log 10 CFU) of ( A ) naftifine-sensitive M. abscessus ATCC 19977 T S (Mab S, blue) strain and naftifine-resistant M. abscessus strain (Mab-Naft R1, red) in wild-type RAW 264.7 macrophages (filled circles) or ( B ) ATG16L1 knockdown macrophages (open circles) treated with naftifine at 0, 5, 10, and 20 µM. Bacterial loads were quantified on days 1 (D1) and 2 (D2) post-infection. ( C and D ) Representative immunoblots showing LC3-I/LC3-II expression and β-actin (loading control) in macrophage lysates at day 1 post-infection with ( C ) Mab-Naft S or ( D ) Mab-Naft R1, treated with indicated naftifine concentrations (μM). Data represent mean ± SEM. Statistical significance was determined by two-way ANOVA. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Knockdown, Infection, Western Blot, Expressing, Control

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: Synergistic interactions between naftifine and β-lactam antibiotics against M. abscessus . Checkerboard assays were performed to evaluate drug interactions between naftifine ( y -axis) and various antibiotics ( x -axis) against M. abscessus ATCC 19977 T smooth variant. Heat maps display the percentage of bacterial growth, with darker blue indicating greater growth. Twofold serial dilutions of each drug were tested in combination, and growth inhibition was assessed after incubation. Naftifine showed indifferent interactions with clarithromycin ( A ) and tigecycline ( E ), additive/partial synergistic effects with amikacin ( B ), but demonstrated synergistic effects when combined with the β-lactam antibiotics cefoxitin ( C ) and imipenem ( D ), particularly at sub-inhibitory concentrations. Synergy was defined as FICI ≤ 0.5, where the combined effect significantly exceeded the sum of individual drug activities. Data were analyzed and plotted using GraphPad Prism version 10.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Variant Assay, Inhibition, Incubation

Frequency of mutational M. abscessus resistance (FoR) to apramycin (APR) and amikacin (AMK). (a) M. abscessus ATCC 19977. (b) M. abscessus NR-44261. All studies were performed on selective LB agar plates incubated at 37 °C for 5 days. Data are represented as scatter plot, the centre bars represent the geometric mean ( n = 3–4 technical replicates per strain and drug concentration tested). The lower limits of quantification (LoQ) defined by ≤ 1 CFU per plate are indicated by dotted lines. Circular symbols at the LoQ are equivalent to one resistant CFU, triangular symbols pointing downward indicate the absence of resistant CFUs and thus a frequency below that LoQ.

Journal: eBioMedicine

Article Title: Multicentre preclinical profiling of apramycin for the treatment of nontuberculous mycobacteria

doi: 10.1016/j.ebiom.2025.106103

Figure Lengend Snippet: Frequency of mutational M. abscessus resistance (FoR) to apramycin (APR) and amikacin (AMK). (a) M. abscessus ATCC 19977. (b) M. abscessus NR-44261. All studies were performed on selective LB agar plates incubated at 37 °C for 5 days. Data are represented as scatter plot, the centre bars represent the geometric mean ( n = 3–4 technical replicates per strain and drug concentration tested). The lower limits of quantification (LoQ) defined by ≤ 1 CFU per plate are indicated by dotted lines. Circular symbols at the LoQ are equivalent to one resistant CFU, triangular symbols pointing downward indicate the absence of resistant CFUs and thus a frequency below that LoQ.

Article Snippet: Dose-dependent killing of planktonic and intracellular NTMs by apramycin (APR) in comparison to amikacin (AMK). (a) Time- and dose-dependent CFU reduction of M. abscessus reference strains ATCC 19977 (smooth) and NR-44261 (rough) in CAMHB (pH 7.4) determined by sampling, plating, and CFU counting at different time points over 120 h. (b) Luminescence based killing kinetics in standard Middlebrook 7H9 (pH 6.7) and in a 7H9 medium that has been buffered with MES to pH 6.0. (c) Dose–response kill curve for stationary-phase M. abscessus ATCC 19977 in caseum surrogate following five days of drug exposure (mean ± SD; n = 3 technical replicates). (d) Dose response curve of intracellular killing of M. abscessus ATCC 19977 by day 3 and of M. avium ATCC 19698 by day 7 (mean ± SD; n = 3 biological replicates).

Techniques: Incubation, Concentration Assay

Dose-dependent killing of planktonic and intracellular NTMs by apramycin (APR) in comparison to amikacin (AMK). (a) Time- and dose-dependent CFU reduction of M. abscessus reference strains ATCC 19977 (smooth) and NR-44261 (rough) in CAMHB (pH 7.4) determined by sampling, plating, and CFU counting at different time points over 120 h. (b) Luminescence based killing kinetics in standard Middlebrook 7H9 (pH 6.7) and in a 7H9 medium that has been buffered with MES to pH 6.0. (c) Dose–response kill curve for stationary-phase M. abscessus ATCC 19977 in caseum surrogate following five days of drug exposure (mean ± SD; n = 3 technical replicates). (d) Dose response curve of intracellular killing of M. abscessus ATCC 19977 by day 3 and of M. avium ATCC 19698 by day 7 (mean ± SD; n = 3 biological replicates). MXF, moxifloxacin; CLA, clarithromycin.

Journal: eBioMedicine

Article Title: Multicentre preclinical profiling of apramycin for the treatment of nontuberculous mycobacteria

doi: 10.1016/j.ebiom.2025.106103

Figure Lengend Snippet: Dose-dependent killing of planktonic and intracellular NTMs by apramycin (APR) in comparison to amikacin (AMK). (a) Time- and dose-dependent CFU reduction of M. abscessus reference strains ATCC 19977 (smooth) and NR-44261 (rough) in CAMHB (pH 7.4) determined by sampling, plating, and CFU counting at different time points over 120 h. (b) Luminescence based killing kinetics in standard Middlebrook 7H9 (pH 6.7) and in a 7H9 medium that has been buffered with MES to pH 6.0. (c) Dose–response kill curve for stationary-phase M. abscessus ATCC 19977 in caseum surrogate following five days of drug exposure (mean ± SD; n = 3 technical replicates). (d) Dose response curve of intracellular killing of M. abscessus ATCC 19977 by day 3 and of M. avium ATCC 19698 by day 7 (mean ± SD; n = 3 biological replicates). MXF, moxifloxacin; CLA, clarithromycin.

Techniques: Comparison, Sampling

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reference strain m abscessus atcc 19977 t (ATCC)

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