HY-148433 Search Results


rmc 6236  (MedChemExpress)
94
MedChemExpress rmc 6236
a , KRASi decrease ACLY mRNA level in a dose-dependent manner. AsPC-1 cells were treated with MRTX1133 <t>or</t> <t>RMC-6236</t> over a two-point dose response for 24 h for RT-qPCR analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test. b , KRASi decrease Cyto AcCoA levels. AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h and the Cyto AcCoA level was measured by LC-MS and normalized by cell number. n = 3 biological replicates. Data shown as the mean ± s.e.m. Welch’s t -test for MRTX1133 analysis and unpaired two-tailed Student’s t -test for RMC-6236 analysis. c - f , KRASi decrease ACLY protein level and induce mitophagy in a dose-dependent manner. KPC ( e ) or AsPC-1 ( c , d , f ) cells treated with MRTX1133 or RMC-6236 over a three-point dose ( c ) or a two-point dose ( d - f ) for 24 h with or without Baf A1 (200 nM). Total cell or Mito lysates for immunoblotting ( c) , cells expressing mt-Keima reporter for flow cytometry analysis ( d ), or qPCR analysis of mtDNA/nDNA ( e , f ). n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( d - f ). g - l , Ace blocks KRASi-induced mitophagy. KPC ( g , h , k ) or AsPC-1 ( i , j , l ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h with or without 10 mM Ace. Total cell or Mito lysates for immunoblotting ( g , i) , cells expressing mt-Keima reporter for flow cytometry analysis ( h , j) , or qPCR analysis of mtDNA/nDNA ( k , l) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( h,j,k,l ). m - p , NLRX1 is required for KRASi-induced mitophagic response. Control (sgNC) or NLRX1 knockout (sg NLRX1 ) KPC ( o ) or AsPC-1 ( m , n , p ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h. Total cell or Mito lysates for immunoblotting ( m ), cells expressing mt-Keima reporter for flow cytometry analysis ( n) , or qPCR analysis of mtDNA/nDNA ( o , p) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test ( n-p) . q , Elevated ROS level in Nlrx1- depleted AsPC-1 cells after KRASi treatment. Control (sgNC) and NLRX1 -depleting (sg NLRX1 ) AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h for CM-H2DCFDA staining by flow cytometry analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. r , NLRX1 depletion and mitophagy inhibitor Mdivi-1 decrease cell viability upon KRASi treatment. IC 50 values calculated based on the dose-response of MRTX1133 or RMC-6236 in control (sgNC) or NLRX1 -depleting (sg NLRX1 ) cells by 3-day (AsPC-1 and A549) or 5-day (KPC) cell-titer-glo assays. n = 3 biological replicates for all analyses, except for KPC cells (MRTX1133, n = 6 biological replicates), A549 cells (Mdivi-1, n = 6 biological replicates), and AsPC-1 cells (sg NLRX1 , n = 4 biological replicates). s , NAC rescues low-dose MRTX1133-induced cell death in Nlrx1 -deficient cells. Control (sgNC) or Nlrx1 -depleting (sg Nlrx1 ) KPC cells were treated with or without 1 nM MRTX1133, and NAC (4 mM) was added on the second day. Four days later, cell viability was determined by cell-titer-glo assays. n = 3 biological replicates. Two-way ANOVA and Bonferroni’s multiple comparisons test. t , Mitophagy inhibitor Mdivi-1 decreases cell viability in KPC cells. Dose-response curves for MRTX1133 in combination with mitophagy inhibitor Mdivi-1 (20 μM) in KPC cells based on 5-day cell-titer-glo assays. IC 50 values are displayed on the top panel. n = 6 biological replicates. u , v , Nlrx1 knockout exacerbates the suppressive effect of MRTX1133 on tumour cell growth in vivo. sgNC and sg Nlrx1 KPC cells were subcutaneously injected in NSG mice for vehicle or MRTX1133 (30 mg per kg, twice a day) treatment when tumour volume reached around 300 mm 3 . Tumour weight ( u ), images ( v ) of KPC-derived allograft in NSG mice. n = 5 mice per group. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. w , MRTX1133 upregulates ROS production in Nlrx1 -deficient tumour. Tumours were harvested after 6 days of indicated treatments. ROS level in tumour tissue sections determined by CM-H2DCFDA staining. n = 5 mice per group. Scale bar, 10 μm.
Rmc 6236, 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
https://www.bioz.com/result/rmc 6236/product/MedChemExpress
Average 94 stars, based on 1 article reviews
rmc 6236 - by Bioz Stars, 2026-02
94/100 stars
  Buy from Supplier

Image Search Results


a , KRASi decrease ACLY mRNA level in a dose-dependent manner. AsPC-1 cells were treated with MRTX1133 or RMC-6236 over a two-point dose response for 24 h for RT-qPCR analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test. b , KRASi decrease Cyto AcCoA levels. AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h and the Cyto AcCoA level was measured by LC-MS and normalized by cell number. n = 3 biological replicates. Data shown as the mean ± s.e.m. Welch’s t -test for MRTX1133 analysis and unpaired two-tailed Student’s t -test for RMC-6236 analysis. c - f , KRASi decrease ACLY protein level and induce mitophagy in a dose-dependent manner. KPC ( e ) or AsPC-1 ( c , d , f ) cells treated with MRTX1133 or RMC-6236 over a three-point dose ( c ) or a two-point dose ( d - f ) for 24 h with or without Baf A1 (200 nM). Total cell or Mito lysates for immunoblotting ( c) , cells expressing mt-Keima reporter for flow cytometry analysis ( d ), or qPCR analysis of mtDNA/nDNA ( e , f ). n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( d - f ). g - l , Ace blocks KRASi-induced mitophagy. KPC ( g , h , k ) or AsPC-1 ( i , j , l ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h with or without 10 mM Ace. Total cell or Mito lysates for immunoblotting ( g , i) , cells expressing mt-Keima reporter for flow cytometry analysis ( h , j) , or qPCR analysis of mtDNA/nDNA ( k , l) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( h,j,k,l ). m - p , NLRX1 is required for KRASi-induced mitophagic response. Control (sgNC) or NLRX1 knockout (sg NLRX1 ) KPC ( o ) or AsPC-1 ( m , n , p ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h. Total cell or Mito lysates for immunoblotting ( m ), cells expressing mt-Keima reporter for flow cytometry analysis ( n) , or qPCR analysis of mtDNA/nDNA ( o , p) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test ( n-p) . q , Elevated ROS level in Nlrx1- depleted AsPC-1 cells after KRASi treatment. Control (sgNC) and NLRX1 -depleting (sg NLRX1 ) AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h for CM-H2DCFDA staining by flow cytometry analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. r , NLRX1 depletion and mitophagy inhibitor Mdivi-1 decrease cell viability upon KRASi treatment. IC 50 values calculated based on the dose-response of MRTX1133 or RMC-6236 in control (sgNC) or NLRX1 -depleting (sg NLRX1 ) cells by 3-day (AsPC-1 and A549) or 5-day (KPC) cell-titer-glo assays. n = 3 biological replicates for all analyses, except for KPC cells (MRTX1133, n = 6 biological replicates), A549 cells (Mdivi-1, n = 6 biological replicates), and AsPC-1 cells (sg NLRX1 , n = 4 biological replicates). s , NAC rescues low-dose MRTX1133-induced cell death in Nlrx1 -deficient cells. Control (sgNC) or Nlrx1 -depleting (sg Nlrx1 ) KPC cells were treated with or without 1 nM MRTX1133, and NAC (4 mM) was added on the second day. Four days later, cell viability was determined by cell-titer-glo assays. n = 3 biological replicates. Two-way ANOVA and Bonferroni’s multiple comparisons test. t , Mitophagy inhibitor Mdivi-1 decreases cell viability in KPC cells. Dose-response curves for MRTX1133 in combination with mitophagy inhibitor Mdivi-1 (20 μM) in KPC cells based on 5-day cell-titer-glo assays. IC 50 values are displayed on the top panel. n = 6 biological replicates. u , v , Nlrx1 knockout exacerbates the suppressive effect of MRTX1133 on tumour cell growth in vivo. sgNC and sg Nlrx1 KPC cells were subcutaneously injected in NSG mice for vehicle or MRTX1133 (30 mg per kg, twice a day) treatment when tumour volume reached around 300 mm 3 . Tumour weight ( u ), images ( v ) of KPC-derived allograft in NSG mice. n = 5 mice per group. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. w , MRTX1133 upregulates ROS production in Nlrx1 -deficient tumour. Tumours were harvested after 6 days of indicated treatments. ROS level in tumour tissue sections determined by CM-H2DCFDA staining. n = 5 mice per group. Scale bar, 10 μm.

Journal: Nature

Article Title: Cytosolic acetyl-coenzyme A is a signalling metabolite to control mitophagy

doi: 10.1038/s41586-025-09745-x

Figure Lengend Snippet: a , KRASi decrease ACLY mRNA level in a dose-dependent manner. AsPC-1 cells were treated with MRTX1133 or RMC-6236 over a two-point dose response for 24 h for RT-qPCR analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test. b , KRASi decrease Cyto AcCoA levels. AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h and the Cyto AcCoA level was measured by LC-MS and normalized by cell number. n = 3 biological replicates. Data shown as the mean ± s.e.m. Welch’s t -test for MRTX1133 analysis and unpaired two-tailed Student’s t -test for RMC-6236 analysis. c - f , KRASi decrease ACLY protein level and induce mitophagy in a dose-dependent manner. KPC ( e ) or AsPC-1 ( c , d , f ) cells treated with MRTX1133 or RMC-6236 over a three-point dose ( c ) or a two-point dose ( d - f ) for 24 h with or without Baf A1 (200 nM). Total cell or Mito lysates for immunoblotting ( c) , cells expressing mt-Keima reporter for flow cytometry analysis ( d ), or qPCR analysis of mtDNA/nDNA ( e , f ). n = 3 biological replicates. Data shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( d - f ). g - l , Ace blocks KRASi-induced mitophagy. KPC ( g , h , k ) or AsPC-1 ( i , j , l ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h with or without 10 mM Ace. Total cell or Mito lysates for immunoblotting ( g , i) , cells expressing mt-Keima reporter for flow cytometry analysis ( h , j) , or qPCR analysis of mtDNA/nDNA ( k , l) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Ordinary one-way ANOVA and Dunnett’s multiple comparisons test ( h,j,k,l ). m - p , NLRX1 is required for KRASi-induced mitophagic response. Control (sgNC) or NLRX1 knockout (sg NLRX1 ) KPC ( o ) or AsPC-1 ( m , n , p ) cells treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h. Total cell or Mito lysates for immunoblotting ( m ), cells expressing mt-Keima reporter for flow cytometry analysis ( n) , or qPCR analysis of mtDNA/nDNA ( o , p) . n = 3 biological replicates. Data are shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test ( n-p) . q , Elevated ROS level in Nlrx1- depleted AsPC-1 cells after KRASi treatment. Control (sgNC) and NLRX1 -depleting (sg NLRX1 ) AsPC-1 cells were treated with MRTX1133 (10 nM), or RMC-6236 (10 nM) for 24 h for CM-H2DCFDA staining by flow cytometry analysis. n = 3 biological replicates. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. r , NLRX1 depletion and mitophagy inhibitor Mdivi-1 decrease cell viability upon KRASi treatment. IC 50 values calculated based on the dose-response of MRTX1133 or RMC-6236 in control (sgNC) or NLRX1 -depleting (sg NLRX1 ) cells by 3-day (AsPC-1 and A549) or 5-day (KPC) cell-titer-glo assays. n = 3 biological replicates for all analyses, except for KPC cells (MRTX1133, n = 6 biological replicates), A549 cells (Mdivi-1, n = 6 biological replicates), and AsPC-1 cells (sg NLRX1 , n = 4 biological replicates). s , NAC rescues low-dose MRTX1133-induced cell death in Nlrx1 -deficient cells. Control (sgNC) or Nlrx1 -depleting (sg Nlrx1 ) KPC cells were treated with or without 1 nM MRTX1133, and NAC (4 mM) was added on the second day. Four days later, cell viability was determined by cell-titer-glo assays. n = 3 biological replicates. Two-way ANOVA and Bonferroni’s multiple comparisons test. t , Mitophagy inhibitor Mdivi-1 decreases cell viability in KPC cells. Dose-response curves for MRTX1133 in combination with mitophagy inhibitor Mdivi-1 (20 μM) in KPC cells based on 5-day cell-titer-glo assays. IC 50 values are displayed on the top panel. n = 6 biological replicates. u , v , Nlrx1 knockout exacerbates the suppressive effect of MRTX1133 on tumour cell growth in vivo. sgNC and sg Nlrx1 KPC cells were subcutaneously injected in NSG mice for vehicle or MRTX1133 (30 mg per kg, twice a day) treatment when tumour volume reached around 300 mm 3 . Tumour weight ( u ), images ( v ) of KPC-derived allograft in NSG mice. n = 5 mice per group. Data shown as the mean ± s.e.m. Two-way ANOVA and Bonferroni’s multiple comparisons test. w , MRTX1133 upregulates ROS production in Nlrx1 -deficient tumour. Tumours were harvested after 6 days of indicated treatments. ROS level in tumour tissue sections determined by CM-H2DCFDA staining. n = 5 mice per group. Scale bar, 10 μm.

Article Snippet: SB (HY-16450), actinomycin D (HY17559), MRTX1133 (HY-134813), RMC-6236 (HY-148439), Torin-1 (HY-13003) and Mdivi-1 (HY-15886) were from MCE.

Techniques: Quantitative RT-PCR, Liquid Chromatography with Mass Spectroscopy, Two Tailed Test, Western Blot, Expressing, Flow Cytometry, Control, Knock-Out, Staining, In Vivo, Injection, Derivative Assay