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AK Scientific perhexiline
IC 50 of a) etomoxir, b) <t>perhexiline,</t> c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.
Perhexiline, supplied by AK Scientific, 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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Average 90 stars, based on 1 article reviews
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Images

1) Product Images from "Direct expression of CPT1a enables a high throughput platform for the discovery of CPT1a modulators"

Article Title: Direct expression of CPT1a enables a high throughput platform for the discovery of CPT1a modulators

Journal: bioRxiv

doi: 10.1101/2024.12.15.628575

IC 50 of a) etomoxir, b) perhexiline, c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.
Figure Legend Snippet: IC 50 of a) etomoxir, b) perhexiline, c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.

Techniques Used: Protein Concentration



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( A ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Etomoxir. Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t test (10 μM vs. control, P = 0.2519; 50 μM vs. control, P = 0.0042; 100 μM vs. control, P = 0.0087; 200 μM vs. control, P = 2.42 × 10 −5 ). n.s. no significance. Scale bar, 50 μm. ( B ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Oxfenicine. Error bars represent mean ± s.e.m. with n = 3 replicates. * P < 0.05, *** P < 0.001; two tailed, unpaired Student’s t test. For Ki67 + /Pax7 + percentage, 2.5 mM vs. control, P = 0.13; 10 mM vs. control, P = 0.0187. For cell count (%), 2.5 mM vs. control, P = 0.00016; 10 mM vs. control, P = 7.97 × 10 −7 ; 2.5 mM vs. 10 mM, P = 0.00017; n.s. no significance. Scale bar, 50 μm. ( C ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or <t>Perhexiline.</t> Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t -test. For Ki67 + /Pax7 + percentage, 2.5 μM vs. control, P = 0.00049; 5 μM vs. control, P = 0.00231; For cell count (%), 2.5 μM vs. control, P = 0.00011; 5 μM vs. control, P = 7.43 × 10 −5 ; 2.5 μM vs. 5 μM, P = 0.0037. Scale bar, 50 μm.
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MRD 3D microtumors reveal specific drug responses toward fatty acid oxidation inhibitors. (A,B) Cell viability changes of naïve and MRD 3D microtumors compared to a DMSO control after a 10‐day treatment with (A) 40 µ m etomoxir; (B) 4 µ m <t>perhexiline</t> ( n = 25–93 3D microtumors from 3 to 7 independent experiments). (C,D) Heatmaps of differentially expressed genes (DEGs) upregulated in etomoxir‐resistant MRD 3D microtumors composed of (C) OVCAR5 and (D) OVCAR‐5/RFP. (E) Confocal images of MRD 3D microtumors (3D MT) at D10 stained with the FAO marker CPT1A (yellow), phalloidin (pink), DAPI (blue). Scale bar = 20 µm. (F) Heatmap of DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5. (G) Confocal images showing the DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5 at day 10: AKR1B10 (green, top left panel), AKR1C2 (green, top right panel), FASN (green, bottom left panel), SCD (green, bottom right panel). The cells were also stained with phalloidin (pink), DAPI (blue). Scale bar = 20 µm.
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MRD 3D microtumors reveal specific drug responses toward fatty acid oxidation inhibitors. (A,B) Cell viability changes of naïve and MRD 3D microtumors compared to a DMSO control after a 10‐day treatment with (A) 40 µ m etomoxir; (B) 4 µ m <t>perhexiline</t> ( n = 25–93 3D microtumors from 3 to 7 independent experiments). (C,D) Heatmaps of differentially expressed genes (DEGs) upregulated in etomoxir‐resistant MRD 3D microtumors composed of (C) OVCAR5 and (D) OVCAR‐5/RFP. (E) Confocal images of MRD 3D microtumors (3D MT) at D10 stained with the FAO marker CPT1A (yellow), phalloidin (pink), DAPI (blue). Scale bar = 20 µm. (F) Heatmap of DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5. (G) Confocal images showing the DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5 at day 10: AKR1B10 (green, top left panel), AKR1C2 (green, top right panel), FASN (green, bottom left panel), SCD (green, bottom right panel). The cells were also stained with phalloidin (pink), DAPI (blue). Scale bar = 20 µm.
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MRD 3D microtumors reveal specific drug responses toward fatty acid oxidation inhibitors. (A,B) Cell viability changes of naïve and MRD 3D microtumors compared to a DMSO control after a 10‐day treatment with (A) 40 µ m etomoxir; (B) 4 µ m <t>perhexiline</t> ( n = 25–93 3D microtumors from 3 to 7 independent experiments). (C,D) Heatmaps of differentially expressed genes (DEGs) upregulated in etomoxir‐resistant MRD 3D microtumors composed of (C) OVCAR5 and (D) OVCAR‐5/RFP. (E) Confocal images of MRD 3D microtumors (3D MT) at D10 stained with the FAO marker CPT1A (yellow), phalloidin (pink), DAPI (blue). Scale bar = 20 µm. (F) Heatmap of DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5. (G) Confocal images showing the DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5 at day 10: AKR1B10 (green, top left panel), AKR1C2 (green, top right panel), FASN (green, bottom left panel), SCD (green, bottom right panel). The cells were also stained with phalloidin (pink), DAPI (blue). Scale bar = 20 µm.
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AK Scientific perhexiline
IC 50 of a) etomoxir, b) <t>perhexiline,</t> c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.
Perhexiline, supplied by AK Scientific, 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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MedChemExpress perhexiline maleate in vitro treatments
IC 50 of a) etomoxir, b) <t>perhexiline,</t> c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.
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Image Search Results


( A ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Etomoxir. Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t test (10 μM vs. control, P = 0.2519; 50 μM vs. control, P = 0.0042; 100 μM vs. control, P = 0.0087; 200 μM vs. control, P = 2.42 × 10 −5 ). n.s. no significance. Scale bar, 50 μm. ( B ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Oxfenicine. Error bars represent mean ± s.e.m. with n = 3 replicates. * P < 0.05, *** P < 0.001; two tailed, unpaired Student’s t test. For Ki67 + /Pax7 + percentage, 2.5 mM vs. control, P = 0.13; 10 mM vs. control, P = 0.0187. For cell count (%), 2.5 mM vs. control, P = 0.00016; 10 mM vs. control, P = 7.97 × 10 −7 ; 2.5 mM vs. 10 mM, P = 0.00017; n.s. no significance. Scale bar, 50 μm. ( C ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Perhexiline. Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t -test. For Ki67 + /Pax7 + percentage, 2.5 μM vs. control, P = 0.00049; 5 μM vs. control, P = 0.00231; For cell count (%), 2.5 μM vs. control, P = 0.00011; 5 μM vs. control, P = 7.43 × 10 −5 ; 2.5 μM vs. 5 μM, P = 0.0037. Scale bar, 50 μm.

Journal: The EMBO Journal

Article Title: Mitochondrial fatty acid oxidation regulates adult muscle stem cell function through modulating metabolic flux and protein acetylation

doi: 10.1038/s44318-025-00397-1

Figure Lengend Snippet: ( A ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Etomoxir. Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t test (10 μM vs. control, P = 0.2519; 50 μM vs. control, P = 0.0042; 100 μM vs. control, P = 0.0087; 200 μM vs. control, P = 2.42 × 10 −5 ). n.s. no significance. Scale bar, 50 μm. ( B ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Oxfenicine. Error bars represent mean ± s.e.m. with n = 3 replicates. * P < 0.05, *** P < 0.001; two tailed, unpaired Student’s t test. For Ki67 + /Pax7 + percentage, 2.5 mM vs. control, P = 0.13; 10 mM vs. control, P = 0.0187. For cell count (%), 2.5 mM vs. control, P = 0.00016; 10 mM vs. control, P = 7.97 × 10 −7 ; 2.5 mM vs. 10 mM, P = 0.00017; n.s. no significance. Scale bar, 50 μm. ( C ) Ki67 immunofluorescence (green) and quantification of percentages of Ki67 + primary myoblasts treated with vehicle control or Perhexiline. Error bars represent mean ± s.e.m. with n = 6–9 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t -test. For Ki67 + /Pax7 + percentage, 2.5 μM vs. control, P = 0.00049; 5 μM vs. control, P = 0.00231; For cell count (%), 2.5 μM vs. control, P = 0.00011; 5 μM vs. control, P = 7.43 × 10 −5 ; 2.5 μM vs. 5 μM, P = 0.0037. Scale bar, 50 μm.

Article Snippet: Perhexiline (maleate) , Cayman Chemical , Cat# 16982.

Techniques: Immunofluorescence, Control, Two Tailed Test, Cell Counting

( A ) Immunofluorescence of MyoG (red) and MF20 (green) and quantification of differentiation and fusion index in primary myoblasts treated with vehicle control or Etomoxir. Error bars represent mean ± s.e.m. with n = 4–6 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t -test. For differentiation index, 50 μM vs. control, P = 0.0057; 100 μM vs. control, P = 0.0013. For fusion index, 50 μM vs. control, P = 0.0021; 100 μM vs. control, P = 0.00032. Scale bar, 500 μm (top); 100 μm (bottom). ( B ) Immunoblots showing relative levels of MF20 and Cpt2 in primary myoblasts treated with vehicle control or Etomoxir (50 µM). ( C ) Immunofluorescence of MyoG (red) and MF20 (green) and quantification of differentiation and fusion index in primary myoblasts treated with vehicle control or Perhexiline (5 µM) and Oxfenicine (2.5 mM). Error bars represent mean ± s.e.m. with n = 3–6 replicates. * P < 0.05, ** P < 0.01; two tailed, unpaired Student’s t test. For differentiation index, Perhexiline vs. control, P = 0.0472; Oxfenicine vs. control, P = 0.012. For fusion index, Perhexiline vs. control, P = 0.0025; Oxfenicine vs. control, P = 0.01052. Scale bar, 200 μm (top); 100 μm (bottom).

Journal: The EMBO Journal

Article Title: Mitochondrial fatty acid oxidation regulates adult muscle stem cell function through modulating metabolic flux and protein acetylation

doi: 10.1038/s44318-025-00397-1

Figure Lengend Snippet: ( A ) Immunofluorescence of MyoG (red) and MF20 (green) and quantification of differentiation and fusion index in primary myoblasts treated with vehicle control or Etomoxir. Error bars represent mean ± s.e.m. with n = 4–6 replicates. ** P < 0.01, *** P < 0.001; two tailed, unpaired Student’s t -test. For differentiation index, 50 μM vs. control, P = 0.0057; 100 μM vs. control, P = 0.0013. For fusion index, 50 μM vs. control, P = 0.0021; 100 μM vs. control, P = 0.00032. Scale bar, 500 μm (top); 100 μm (bottom). ( B ) Immunoblots showing relative levels of MF20 and Cpt2 in primary myoblasts treated with vehicle control or Etomoxir (50 µM). ( C ) Immunofluorescence of MyoG (red) and MF20 (green) and quantification of differentiation and fusion index in primary myoblasts treated with vehicle control or Perhexiline (5 µM) and Oxfenicine (2.5 mM). Error bars represent mean ± s.e.m. with n = 3–6 replicates. * P < 0.05, ** P < 0.01; two tailed, unpaired Student’s t test. For differentiation index, Perhexiline vs. control, P = 0.0472; Oxfenicine vs. control, P = 0.012. For fusion index, Perhexiline vs. control, P = 0.0025; Oxfenicine vs. control, P = 0.01052. Scale bar, 200 μm (top); 100 μm (bottom).

Article Snippet: Perhexiline (maleate) , Cayman Chemical , Cat# 16982.

Techniques: Immunofluorescence, Control, Two Tailed Test, Western Blot

Reagents and tools table

Journal: The EMBO Journal

Article Title: Mitochondrial fatty acid oxidation regulates adult muscle stem cell function through modulating metabolic flux and protein acetylation

doi: 10.1038/s44318-025-00397-1

Figure Lengend Snippet: Reagents and tools table

Article Snippet: Perhexiline (maleate) , Cayman Chemical , Cat# 16982.

Techniques: Produced, Ex Vivo, In Vitro, Sequencing, Red Blood Cell Lysis, Modification, Saline, Blocking Assay, Plasmid Preparation, Protease Inhibitor, Reverse Transcription, Isolation, Bicinchoninic Acid Protein Assay, Western Blot, In Situ, Fluorescence, Detection Assay, TUNEL Assay, Software, Microscopy, Mass Spectrometry, Liquid Chromatography

MRD 3D microtumors reveal specific drug responses toward fatty acid oxidation inhibitors. (A,B) Cell viability changes of naïve and MRD 3D microtumors compared to a DMSO control after a 10‐day treatment with (A) 40 µ m etomoxir; (B) 4 µ m perhexiline ( n = 25–93 3D microtumors from 3 to 7 independent experiments). (C,D) Heatmaps of differentially expressed genes (DEGs) upregulated in etomoxir‐resistant MRD 3D microtumors composed of (C) OVCAR5 and (D) OVCAR‐5/RFP. (E) Confocal images of MRD 3D microtumors (3D MT) at D10 stained with the FAO marker CPT1A (yellow), phalloidin (pink), DAPI (blue). Scale bar = 20 µm. (F) Heatmap of DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5. (G) Confocal images showing the DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5 at day 10: AKR1B10 (green, top left panel), AKR1C2 (green, top right panel), FASN (green, bottom left panel), SCD (green, bottom right panel). The cells were also stained with phalloidin (pink), DAPI (blue). Scale bar = 20 µm.

Journal: Advanced Healthcare Materials

Article Title: 3D Microtumors Representing Ovarian Cancer Minimal Residual Disease Respond to the Fatty Acid Oxidation Inhibitor Perhexiline

doi: 10.1002/adhm.202404072

Figure Lengend Snippet: MRD 3D microtumors reveal specific drug responses toward fatty acid oxidation inhibitors. (A,B) Cell viability changes of naïve and MRD 3D microtumors compared to a DMSO control after a 10‐day treatment with (A) 40 µ m etomoxir; (B) 4 µ m perhexiline ( n = 25–93 3D microtumors from 3 to 7 independent experiments). (C,D) Heatmaps of differentially expressed genes (DEGs) upregulated in etomoxir‐resistant MRD 3D microtumors composed of (C) OVCAR5 and (D) OVCAR‐5/RFP. (E) Confocal images of MRD 3D microtumors (3D MT) at D10 stained with the FAO marker CPT1A (yellow), phalloidin (pink), DAPI (blue). Scale bar = 20 µm. (F) Heatmap of DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5. (G) Confocal images showing the DEGs upregulated in perhexiline‐resistant MRD 3D microtumors composed of OVCAR5 at day 10: AKR1B10 (green, top left panel), AKR1C2 (green, top right panel), FASN (green, bottom left panel), SCD (green, bottom right panel). The cells were also stained with phalloidin (pink), DAPI (blue). Scale bar = 20 µm.

Article Snippet: Etomoxir sodium salt (Stratech, #S8244‐SEL) was dissolved in DMSO to prepare a 40 m m stock solution, which was diluted in cell medium to a final concentration of 40 μ m . Perhexiline (Cambridge Bioscience, #CAY16982) was dissolved in DMSO to prepare a 4 m m perhexiline stock solution, which was diluted in cell medium to a final concentration of 4 μ m . DMSO was added to cell medium at a 1:1000 volume ratio for the control group.

Techniques: Control, Staining, Marker

IC 50 of a) etomoxir, b) perhexiline, c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.

Journal: bioRxiv

Article Title: Direct expression of CPT1a enables a high throughput platform for the discovery of CPT1a modulators

doi: 10.1101/2024.12.15.628575

Figure Lengend Snippet: IC 50 of a) etomoxir, b) perhexiline, c) chlorpromazine. A series of concentrations of each compound was used accordingly. We used the same amount of human CPT1a pellet solution with a protein concentration of 0.67 μg/μL, adding 2 μL of protein in each group.

Article Snippet: Two previously reported CPT1 inhibitors, etomoxir sodium salt (Cayman Chemical, Cat. #11969) and perhexiline (AK Scientific, Cat. #X4611), were used to validate the potential of this assay as a platform to screen for novel CPT1 inhibitors.

Techniques: Protein Concentration