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entinostat ms 275 (MedChemExpress)

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MedChemExpress entinostat ms 275
Entinostat Ms 275, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 103 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/entinostat ms 275/product/MedChemExpress
Average 95 stars, based on 103 article reviews

entinostat ms 275 - by Bioz Stars, 2026-06

95/100 stars

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MS-275 recovers skeletal muscle atrophy in db/db mice. (A) Representative axial magnetic resonance imaging scans of hindlimb muscles from control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) Representative images and weights of gastrocnemius (GA) and tibialis anterior (TA) muscles from each group. (C) Hematoxylin and eosin (H&E) staining and quantification of muscle fiber cross-sectional area (CSA) in GA and TA muscles. CSAs were quantified using ImageJ software. Data are presented as mean ± SEM. Effect sizes (η²): (A) 0.872; (B) GA = 0.838, TA = 0.631; (C) GA = 0.912, TA = 0.781. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control; # p < 0.05, ## p < 0.01, and ### p < 0.001 vs. diabetic muscle atrophy group. SEM, standard error of the mean.

Journal: Frontiers in Endocrinology

Article Title: Epigenetic inhibition of class I histone deacetylases by MS-275 attenuates diabetic skeletal muscle atrophy via Akt/ARK5–FoxO and myostatin–Smad signaling

doi: 10.3389/fendo.2026.1788603

Figure Lengend Snippet: MS-275 recovers skeletal muscle atrophy in db/db mice. (A) Representative axial magnetic resonance imaging scans of hindlimb muscles from control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) Representative images and weights of gastrocnemius (GA) and tibialis anterior (TA) muscles from each group. (C) Hematoxylin and eosin (H&E) staining and quantification of muscle fiber cross-sectional area (CSA) in GA and TA muscles. CSAs were quantified using ImageJ software. Data are presented as mean ± SEM. Effect sizes (η²): (A) 0.872; (B) GA = 0.838, TA = 0.631; (C) GA = 0.912, TA = 0.781. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control; # p < 0.05, ## p < 0.01, and ### p < 0.001 vs. diabetic muscle atrophy group. SEM, standard error of the mean.

Article Snippet: The control and diabetic muscle atrophy groups received intraperitoneal injections of dimethyl sulfoxide (DMSO; Sigma-Aldrich, St. Louis, MO, USA), whereas the treatment group received MS-275 (entinostat, a class I histone deacetylase inhibitor; 10 mg/kg; MedChemExpress, Monmouth Junction, NJ, USA).

Techniques: Magnetic Resonance Imaging, Muscles, Control, Staining, Software

MS-275 ameliorates skeletal muscle inflammation in db/db mice. (A) F4/80 immunohistochemical staining of gastrocnemius (GA) and tibialis anterior (TA) muscles to assess macrophage infiltration in control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) mRNA expression levels of pro-inflammatory cytokines TNF-α and IL-1β in GA muscle determined by quantitative reverse transcription PCR (qRT-PCR). (C) Plasma TNF-α concentrations measured by enzyme-linked immunosorbent assay (ELISA). (D) Western blot analysis of phosphorylated p65 (p-p65) and total p65 in GA muscle. Relative protein levels were quantified using ImageJ software. Data are presented as mean ± SEM. Effect size (η²) for plasma TNF-α is 0.974. * p < 0.05, *** p < 0.001 vs. control; # p < 0.05 and ## p <0.01 vs. diabetic muscle atrophy group. TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; SEM, standard error of the mean.

Journal: Frontiers in Endocrinology

Article Title: Epigenetic inhibition of class I histone deacetylases by MS-275 attenuates diabetic skeletal muscle atrophy via Akt/ARK5–FoxO and myostatin–Smad signaling

doi: 10.3389/fendo.2026.1788603

Figure Lengend Snippet: MS-275 ameliorates skeletal muscle inflammation in db/db mice. (A) F4/80 immunohistochemical staining of gastrocnemius (GA) and tibialis anterior (TA) muscles to assess macrophage infiltration in control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) mRNA expression levels of pro-inflammatory cytokines TNF-α and IL-1β in GA muscle determined by quantitative reverse transcription PCR (qRT-PCR). (C) Plasma TNF-α concentrations measured by enzyme-linked immunosorbent assay (ELISA). (D) Western blot analysis of phosphorylated p65 (p-p65) and total p65 in GA muscle. Relative protein levels were quantified using ImageJ software. Data are presented as mean ± SEM. Effect size (η²) for plasma TNF-α is 0.974. * p < 0.05, *** p < 0.001 vs. control; # p < 0.05 and ## p <0.01 vs. diabetic muscle atrophy group. TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; SEM, standard error of the mean.

Techniques: Immunohistochemical staining, Staining, Muscles, Control, Expressing, Reverse Transcription, Quantitative RT-PCR, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Western Blot, Software

MS-275 attenuates muscle atrophy–related signaling via Smad2/3 and Akt/ARK5 pathways in db/db mice. (A) Plasma myostatin concentrations measured by enzyme-linked immunosorbent assay (ELISA) in control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) Western blot analysis of muscle-specific RING-finger protein 1 (MuRF1) and atrogin-1 in gastrocnemius (GA) muscle. (C) Western blot analysis of suppressor of mothers against decapentaplegic homolog (Smad) 2, Smad3, Smad4, and their phosphorylated forms. (D) Western blot analysis of protein kinase B (Akt) and AMP-activated protein kinase family member 5 (ARK5) phosphorylation. (E) Western blot analysis of Forkhead box O (FoxO) 1 and FoxO3 phosphorylation. Relative protein levels were quantified using ImageJ software. Data are presented as mean ± SEM. Effect size (η²) for plasma myostatin is 0.928. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control; # p < 0.05, ## p < 0.01, and ### p < 0.001 vs. diabetic muscle atrophy group. TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; SEM, standard error of the mean.

Journal: Frontiers in Endocrinology

Article Title: Epigenetic inhibition of class I histone deacetylases by MS-275 attenuates diabetic skeletal muscle atrophy via Akt/ARK5–FoxO and myostatin–Smad signaling

doi: 10.3389/fendo.2026.1788603

Figure Lengend Snippet: MS-275 attenuates muscle atrophy–related signaling via Smad2/3 and Akt/ARK5 pathways in db/db mice. (A) Plasma myostatin concentrations measured by enzyme-linked immunosorbent assay (ELISA) in control ( C57BL/6J ), diabetic muscle atrophy ( db/db ), and MS-275–treated db/db mice. (B) Western blot analysis of muscle-specific RING-finger protein 1 (MuRF1) and atrogin-1 in gastrocnemius (GA) muscle. (C) Western blot analysis of suppressor of mothers against decapentaplegic homolog (Smad) 2, Smad3, Smad4, and their phosphorylated forms. (D) Western blot analysis of protein kinase B (Akt) and AMP-activated protein kinase family member 5 (ARK5) phosphorylation. (E) Western blot analysis of Forkhead box O (FoxO) 1 and FoxO3 phosphorylation. Relative protein levels were quantified using ImageJ software. Data are presented as mean ± SEM. Effect size (η²) for plasma myostatin is 0.928. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control; # p < 0.05, ## p < 0.01, and ### p < 0.001 vs. diabetic muscle atrophy group. TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; SEM, standard error of the mean.

Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Western Blot, Phospho-proteomics, Software

Proposed mechanisms underlying the protective effects of MS-275 against diabetic muscle atrophy. IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor alpha; Smad, suppressor of mothers against decapentaplegic homolog; Akt, protein kinase B; ARK5, AMP-activated protein kinase family member 5; FoxO, forkhead box O; MuRF1, muscle-specific RING-finger protein 1.

Journal: Frontiers in Endocrinology

Article Title: Epigenetic inhibition of class I histone deacetylases by MS-275 attenuates diabetic skeletal muscle atrophy via Akt/ARK5–FoxO and myostatin–Smad signaling

doi: 10.3389/fendo.2026.1788603

Figure Lengend Snippet: Proposed mechanisms underlying the protective effects of MS-275 against diabetic muscle atrophy. IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor alpha; Smad, suppressor of mothers against decapentaplegic homolog; Akt, protein kinase B; ARK5, AMP-activated protein kinase family member 5; FoxO, forkhead box O; MuRF1, muscle-specific RING-finger protein 1.

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Effects of epigenetic inhibitors on IL-1β–induced NUB1 expression in RA and OA fibroblast-like synoviocytes (FLS). RA and OA FLS were pretreated with epigenetic inhibitors and subsequently stimulated with IL-1β (2 ng/mL). NUB1 mRNA expression was quantified by qRT-PCR. Fold change was calculated as the ratio of NUB1 mRNA expression in IL-1β–stimulated cells to the corresponding unstimulated control; specifically, DMSO alone for the IL-1/DMSO condition and the inhibitor-alone control for inhibitor-treated conditions. ( a ) 5-aza-deoxycytidine (5-aza-dC; DNA methyltransferase inhibitor). RA and OA FLS were treated with 5-aza-dC for 14 days prior to stimulation with IL-1β (n = 7 each). 5-aza-dC partially reduced the difference in IL-1β–induced NUB1 expression between RA and OA. Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA ( p = 0.024). Following 5-aza-dC treatment, the magnitude of the OA–RA difference was no longer statistically significant ( p = 0.488), indicating partial attenuation of the baseline RA–OA difference. ( b ) EPZ6438 (EZH2 inhibitor; histone methylation inhibitor). RA and OA FLS were treated with EPZ6438 for 12 or 24 hours before IL-1β stimulation (n = 5 each). treatment with EPZ6438 partially reversed the difference in IL-1β–induced NUB1 expression between RA and OA. Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA. This difference was no longer significant after EPZ6438 treatment at 12 h ( p = 0.329) or 24 h ( p = 0.512). ( c ) Left panel: ITF2357 (pan-HDAC inhibitor); Right panel: MS275 (HDAC1/3 selective inhibitor). RA and OA FLS were treated with each HDAC inhibitor for 12 or 24 hours, followed by IL-1β stimulation (ITF2357; n = 5 each, MS275; n = 6 each). Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA in the ITF2357 panel. Following ITF2357 treatment, the OA–RA difference was no longer statistically significant at 12 h ( p = 0.596) or 24 h ( p = 0.072). Under control conditions, IL-1β–induced NUB1 expression was also significantly higher in OA than in RA in the MS275 panel. Following MS275 treatment, the OA–RA difference was no longer statistically significant at either 12 h ( p = 0.944) or 24 h ( p = 0.846). These data indicate that histone modifications are required for differential induction of NUB1 in OA compared with RA. Circles and squares represent mean fold change for OA and RA FLS, respectively. Statistical analysis was performed at each time point and condition performed by comparing the fold change values between RA and OA FLS using unpaired t test with Welch’s correction (* p < 0.05, ** p < 0.01).

Journal: Scientific Reports

Article Title: Altered fibroblast-like synoviocyte epigenetics is responsible for deficient NUB1 expression in rheumatoid arthritis

doi: 10.1038/s41598-026-38420-y

Figure Lengend Snippet: Effects of epigenetic inhibitors on IL-1β–induced NUB1 expression in RA and OA fibroblast-like synoviocytes (FLS). RA and OA FLS were pretreated with epigenetic inhibitors and subsequently stimulated with IL-1β (2 ng/mL). NUB1 mRNA expression was quantified by qRT-PCR. Fold change was calculated as the ratio of NUB1 mRNA expression in IL-1β–stimulated cells to the corresponding unstimulated control; specifically, DMSO alone for the IL-1/DMSO condition and the inhibitor-alone control for inhibitor-treated conditions. ( a ) 5-aza-deoxycytidine (5-aza-dC; DNA methyltransferase inhibitor). RA and OA FLS were treated with 5-aza-dC for 14 days prior to stimulation with IL-1β (n = 7 each). 5-aza-dC partially reduced the difference in IL-1β–induced NUB1 expression between RA and OA. Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA ( p = 0.024). Following 5-aza-dC treatment, the magnitude of the OA–RA difference was no longer statistically significant ( p = 0.488), indicating partial attenuation of the baseline RA–OA difference. ( b ) EPZ6438 (EZH2 inhibitor; histone methylation inhibitor). RA and OA FLS were treated with EPZ6438 for 12 or 24 hours before IL-1β stimulation (n = 5 each). treatment with EPZ6438 partially reversed the difference in IL-1β–induced NUB1 expression between RA and OA. Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA. This difference was no longer significant after EPZ6438 treatment at 12 h ( p = 0.329) or 24 h ( p = 0.512). ( c ) Left panel: ITF2357 (pan-HDAC inhibitor); Right panel: MS275 (HDAC1/3 selective inhibitor). RA and OA FLS were treated with each HDAC inhibitor for 12 or 24 hours, followed by IL-1β stimulation (ITF2357; n = 5 each, MS275; n = 6 each). Under control conditions, IL-1β–induced NUB1 expression was significantly higher in OA than in RA in the ITF2357 panel. Following ITF2357 treatment, the OA–RA difference was no longer statistically significant at 12 h ( p = 0.596) or 24 h ( p = 0.072). Under control conditions, IL-1β–induced NUB1 expression was also significantly higher in OA than in RA in the MS275 panel. Following MS275 treatment, the OA–RA difference was no longer statistically significant at either 12 h ( p = 0.944) or 24 h ( p = 0.846). These data indicate that histone modifications are required for differential induction of NUB1 in OA compared with RA. Circles and squares represent mean fold change for OA and RA FLS, respectively. Statistical analysis was performed at each time point and condition performed by comparing the fold change values between RA and OA FLS using unpaired t test with Welch’s correction (* p < 0.05, ** p < 0.01).

Article Snippet: For epigenetic modulation experiments, we used the EZH2 inhibitor EPZ6438 (Tazemetostat; Selleck Chemicals), the pan-HDAC inhibitor ITF-2357 (givinostat; Selleck Chemicals), and the selective HDAC1/3 inhibitor MS-275 (entinostat; Selleck Chemicals), as previously described in synovial fibroblast studies .

Techniques: Expressing, Quantitative RT-PCR, Control, Methylation

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