compound 991 Search Results


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SpiroChem ag compound 991
Compound 991, supplied by SpiroChem ag, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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LC Laboratories compound 991
Compound 991, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Metabasis Therapeutics cyclic benzimidazole derivative compound 991
Cyclic Benzimidazole Derivative Compound 991, supplied by Metabasis Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SpiroChem ag ampk activator compound 991 (ex229)
GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( <xref ref-type=Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001). " width="250" height="auto" />
Ampk Activator Compound 991 (Ex229), supplied by SpiroChem ag, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/compound+991/adenosine+monophosphate+activated+protein+kinase++ampk++activator+compound+991++ex229/pmc10999543-39-2-11
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AstraZeneca ltd compound 991
GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( <xref ref-type=Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001). " width="250" height="auto" />
Compound 991, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/compound+991/compound+991/10__1042_slash_bsr20180242-44-0-5
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Metabasis Therapeutics compound 991
GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( <xref ref-type=Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001). " width="250" height="auto" />
Compound 991, supplied by Metabasis Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/compound+991/compound+991/pm28502587-39-0-17
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Adooq Bioscience LLC compound 991
GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( <xref ref-type=Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001). " width="250" height="auto" />
Compound 991, supplied by Adooq Bioscience LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/compound+991/compound+991/pm32434052-49-13-15
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Informationex229 (compound 991) EX229 (compound 991) is a potent AMPK activator that is 5-10-fold more potent than A769662 in activating AMPK.TargetsAMPKIn vitroEX229 activates AMPK in incubated rat epitrochlearis skeletal muscle and incubation of rat skeletal
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GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( <xref ref-type=Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001). " width="100%" height="100%">

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Identification of kinase modulators as host-directed therapeutics against intracellular methicillin-resistant Staphylococcus aureus

doi: 10.3389/fcimb.2024.1367938

Figure Lengend Snippet: GW296115X activates AMPK resulting in autophagosome formation and elimination of intracellular MRSA. (A) Chemical structure of GW296115X. (B, C) GW296115X was tested at different concentrations to determine its antimicrobial potency (B) and level of cytoxicity (C) in MRSA-infected HeLa cells. (D) The KinMap kinase phylogenetic tree shows the kinase inhibition profile of GW296115X as determined by Caliper assay ( Elkins et al., 2016 ). Each circle represents a kinase target that is inhibited > 50% at 0.1 µM (purple) or 1 µM (blue) concentration. (E) Phosphorylation of ACC1 at Ser80, a direct target of AMPK, was determined by flow cytometry and expressed as fold change in geometric mean fluorescent intensity (gMFI) compared to untreated HeLa cells. The AMPK-activating compound 991 was used as a positive control. (F) Phosphorylation of AMPK at Thr172 was determined by western blot and expressed as the ratio between phosphorylated and unphosphorylated AMPK. (G) Autophagosome formation was determined by western blot and expressed as the ratio between lipidated, membrane-bound LC3 (LC3-II) and cytosolic LC3 (LC3-I). Abbreviations: BAF = bafilomycin A1; RAP = rapamycin. The combination of lysosome inhibitor bafilomycin A1 and mTOR -inhibitor rapamycin results was used as a positive control that results in LC3-II accumulation. (H, I) The interaction between bafilomycin A1 and GW296115X and their effect against intracellular MRSA (H) and host cell viability (I) were determined. (J, K) The effect of two other autophagy-inducing compounds 991 and rapamycin against intracellular MRSA (J) and host cell viability (K) were determined. Each datapoint represents the results of an independent experiment. Statistical significance of observed differences was tested in comparison to the DMSO controls ( *p < 0 .05; * *p < 0 .01; *** p < 0.001).

Article Snippet: Adenosine monophosphate-activated protein kinase (AMPK) activator compound 991 (ex229) ( ) (Spirochem, Basel, Switzerland; used at 25 μM) was kindly shared by Eline Brombacher and Dr. Bart Everts (Leiden university Medical Center, Leiden, Netherlands).

Techniques: Infection, Inhibition, Concentration Assay, Flow Cytometry, Positive Control, Western Blot, Membrane, Comparison