hdac inhibitor entinostat ms 275  (MedChemExpress)

Journal: Neuro-oncology

Article Title: The CoREST complex inhibitor, corin, decreases tumor growth, increases cellular differentiation and extends lifespan in ATRT xenograft models

doi: 10.1093/neuonc/noag160

Figure Lengend Snippet: (A) Dose-response curves for ATRT cell lines treated with corin for 72 h (n=3). (B) Relative cell viability of ATRT cell lines treated with corin versus the HDAC inhibitor, entinostat/ MS-275 (n=3). (C) Table showing comparative IC 50 s of corin and entinostat in ATRT cell lines sorted by molecular subtype. IC 50 was calculated based on the total viable cell count relative to DMSO in ATRT cell lines. (D) BrdU immunostaining and quantification of ATRT cells treated with DMSO or corin (n=5). Scale 50 μm. (E) Cleaved caspase 3 (CC3) immunostaining for apoptosis and quantification of ATRT cells treated with DMSO versus corin (n=5). Scale 50 μm. (F) MUSE Annexin V/ 7-AAD assay of ATRT cells treated with DMSO or corin (n=3). (G) Quantification of Annexin V apoptosis assay for corin treatment of ATRT cells in (F). Data is presented as fold change of the total number of ATRT cells undergoing apoptosis following corin treatment relative to DMSO. (H) Western blot of cPARP expression in ATRT cells following 72 h treatment with DMSO versus corin (n=3). The band density normalized to beta actin and relative to DMSO is shown below each band. Statistical Analysis: unpaired, two-tailed student’s t test. All data represents mean ± SD. ** p ≤ 0.01; *** p ≤ 0.001.

Article Snippet: The HDAC inhibitor entinostat/MS-275 (Cat# HY-12163) and corin (Cat# HY-111048) were purchased from MedChemExpress (NJ, USA).

Techniques: In Vitro, Cell Characterization, Immunostaining, Apoptosis Assay, Western Blot, Expressing, Analysis, Two Tailed Test

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

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.

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

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.

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

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.

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: