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bazedoxifene acetate bza  (MedChemExpress)


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    Structured Review

    MedChemExpress bazedoxifene acetate bza
    a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or <t>bazedoxifene</t> <t>acetate</t> <t>(BZA)</t> ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.
    Bazedoxifene Acetate Bza, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Mitochondrial vulnerability underlies myocarditis from COVID-19 mRNA vaccine"

    Article Title: Mitochondrial vulnerability underlies myocarditis from COVID-19 mRNA vaccine

    Journal: Nature Communications

    doi: 10.1038/s41467-026-71295-1

    a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or bazedoxifene acetate (BZA) ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.
    Figure Legend Snippet: a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or bazedoxifene acetate (BZA) ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.

    Techniques Used: Two Tailed Test

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    Concentration Assay:

    Article Title: IL-6/gp130/STAT3 signaling contributed to the activation of the PERK arm of the unfolded protein response in response to chronic β-adrenergic stimulation.
    Article Snippet: Prolonged activation of the PERK branch of the unfolded protein response (UPR) promotes cardiomyocytes apoptosis in response to chronic β-adrenergic stimulation.. STAT3 plays a critical role in β-adrenergic functions in the heart.. However, whether STAT3 contributed to β-adrenoceptor-mediated PERK activation and how β-adrenergic signaling activates STAT3 remains unclear.

    other:

    Article Title: Bazedoxifene reverses sexually dimorphic autistic-like abnormalities in biallelic MDGA1-mutant mice
    Article Snippet: The following drugs were commercially purchased: Bazedoxifene acetate (Cat# HY-A0036) and Fulvestrant (Cat# HY-13636) from MedChemExpress (MCE); CNQX (Cat# 0190), D-AP5 (Cat# 0106) and picrotoxin (Cat# 1128) from Tocris Bioscience; Tetrodotoxin (TTX; Cat# 14964) from Cayman Chemical; and 2,2,2-tribromoethyl alcohol (Cat# T48402 ) from Sigma-Aldrich.

    Article Title: Bazedoxifene reverses sexually dimorphic autistic-like abnormalities in biallelic MDGA1-mutant mice.
    Article Snippet: The following drugs were commercially purchased: Bazedoxifene acetate (Cat# HY-A0036) and Fulvestrant (Cat# HY-13636) from MedChemExpress (MCE); CNQX (Cat# 0190), D-AP5 (Cat# 0106) and picrotoxin (Cat# 1128) from Tocris Bioscience; Tetrodotoxin (TTX; Cat# 14964) from Cayman Chemical; and 2,2,2-tribromoethyl alcohol (Cat# T48402) from Sigma-Aldrich.



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    94
    MedChemExpress bazedoxifene acetate bza
    a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or <t>bazedoxifene</t> <t>acetate</t> <t>(BZA)</t> ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.
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    ( A ) Schematic illustrating the experimental paradigm. Adult male control and Mdga1 Y636C/E751Q KI mice were administered <t>bazedoxifene</t> (BZD; 4.1 mg/kg, intraperitoneally) or vehicle (sham). Six hours post-treatment, the mice were subjected to biochemical, electrophysiological, and behavioral analyses. ( B , C ) Semi-quantitative immunoblotting of hippocampal synaptic proteins, including Nlgn2, GABA A receptor subunit, VGAT, and gephyrin from BZD- or sham-treated mice. β-actin was used as a loading control for normalization. Quantification of normalized protein levels ( C ) revealed that BZD rescued the enhanced expression of synaptic proteins observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 6 per group; (Nlgn2) * P = 0.0220, # P = 0.0313; (GABA A Rγ2) ** P = 0.0021, # P = 0.0495; (VGAT) ** P = 0.0059, # P = 0.0343; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( D , E ) Representative immunoblots ( D ) and quantification ( E ) of phosphorylated SynI, SynIIa, and SynIIb proteins obtained via immunoprecipitation with anti-phospho-serine antibody and normalized to total Syn levels. BZD significantly restored phospho-SynII levels in KI hippocampi. Data are means ± SEMs ( n = 4 independent experiments; (SynIIa) **P = 0.0010, ## P = 0.0019; (SynIIb) # P = 0.0441; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( F , G ) ASRs ( F ) and PPI of ASR ( G ) in adult male control and Mdga1 Y636C/E751Q mice given BZD or sham treatment. BZD treatment reversed the reduced ASR in Mdga1 Y636C/E751Q KI mice, but failed to rescue the deficits in PPI. Data are presented as means ± SEMs ( n = 20–21 mice/group; ( F ) * P = 0.0444 (115 dB), * P = 0.0281 (120 dB), # P = 0.0344 (120 dB); ( G ) * P = 0.0195 (73 dB), * P = 0.0205 (76 dB), * P = 0.0429 (79 dB); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( H – K ) USVs recorded from socially isolated adult male mice. Representative traces are shown in ( H ). BZD treatment normalized the increased number of USV calls ( I ) observed in Mdga1 Y636C/E751Q KI mice. Call length ( J ) was not significantly altered across groups. The altered distribution of call types in Mdga1 Y636C/E751Q KI mice was also partially rescued by BZD, including restoration of the reduced proportion of complex trill calls ( K ). Data are means ± SEMs ( n = 9–10 mice/group; ( I ) * P = 0.0323, # P = 0.0456; ( K ) ** P = 0.0089, ## P = 0.0045; # indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( L – P ) Electrophysiological recordings of dendritic eIPSCs in CA1 pyramidal neurons at P56. Representative traces ( L , O ) and quantification of I–O responses ( M , N ) and paired-pulse ratio (PPR; P ) revealed that BZD rescued the increased inhibitory input strength and the presynaptic release probability abnormalities observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 14–21 cells/group; ( M ) (30 μA) ** P = 0.0065 (vs. MI-KI Sham ), ## P = 0.0064 (vs. MI-KI BZD ); (40 μA) ### P = 0.0003 (vs. Ctrl BZD ), *** P = 0.0001 (vs. MI-KI Sham ), ### P = 0.0004 (vs. MI-KI BZD ); (50 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); (60 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); ( N ) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. M1-KI sham ); ( P ) ### P = 0.0004 (vs. Ctrl BZD ), ** P = 0.0010 (vs. M1-KI sham ), ## P = 0.0072 (vs. MI-KI BZD ); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). .
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    ( A ) Schematic illustrating the experimental paradigm. Adult male control and Mdga1 Y636C/E751Q KI mice were administered <t>bazedoxifene</t> (BZD; 4.1 mg/kg, intraperitoneally) or vehicle (sham). Six hours post-treatment, the mice were subjected to biochemical, electrophysiological, and behavioral analyses. ( B , C ) Semi-quantitative immunoblotting of hippocampal synaptic proteins, including Nlgn2, GABA A receptor subunit, VGAT, and gephyrin from BZD- or sham-treated mice. β-actin was used as a loading control for normalization. Quantification of normalized protein levels ( C ) revealed that BZD rescued the enhanced expression of synaptic proteins observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 6 per group; (Nlgn2) * P = 0.0220, # P = 0.0313; (GABA A Rγ2) ** P = 0.0021, # P = 0.0495; (VGAT) ** P = 0.0059, # P = 0.0343; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( D , E ) Representative immunoblots ( D ) and quantification ( E ) of phosphorylated SynI, SynIIa, and SynIIb proteins obtained via immunoprecipitation with anti-phospho-serine antibody and normalized to total Syn levels. BZD significantly restored phospho-SynII levels in KI hippocampi. Data are means ± SEMs ( n = 4 independent experiments; (SynIIa) **P = 0.0010, ## P = 0.0019; (SynIIb) # P = 0.0441; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( F , G ) ASRs ( F ) and PPI of ASR ( G ) in adult male control and Mdga1 Y636C/E751Q mice given BZD or sham treatment. BZD treatment reversed the reduced ASR in Mdga1 Y636C/E751Q KI mice, but failed to rescue the deficits in PPI. Data are presented as means ± SEMs ( n = 20–21 mice/group; ( F ) * P = 0.0444 (115 dB), * P = 0.0281 (120 dB), # P = 0.0344 (120 dB); ( G ) * P = 0.0195 (73 dB), * P = 0.0205 (76 dB), * P = 0.0429 (79 dB); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( H – K ) USVs recorded from socially isolated adult male mice. Representative traces are shown in ( H ). BZD treatment normalized the increased number of USV calls ( I ) observed in Mdga1 Y636C/E751Q KI mice. Call length ( J ) was not significantly altered across groups. The altered distribution of call types in Mdga1 Y636C/E751Q KI mice was also partially rescued by BZD, including restoration of the reduced proportion of complex trill calls ( K ). Data are means ± SEMs ( n = 9–10 mice/group; ( I ) * P = 0.0323, # P = 0.0456; ( K ) ** P = 0.0089, ## P = 0.0045; # indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( L – P ) Electrophysiological recordings of dendritic eIPSCs in CA1 pyramidal neurons at P56. Representative traces ( L , O ) and quantification of I–O responses ( M , N ) and paired-pulse ratio (PPR; P ) revealed that BZD rescued the increased inhibitory input strength and the presynaptic release probability abnormalities observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 14–21 cells/group; ( M ) (30 μA) ** P = 0.0065 (vs. MI-KI Sham ), ## P = 0.0064 (vs. MI-KI BZD ); (40 μA) ### P = 0.0003 (vs. Ctrl BZD ), *** P = 0.0001 (vs. MI-KI Sham ), ### P = 0.0004 (vs. MI-KI BZD ); (50 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); (60 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); ( N ) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. M1-KI sham ); ( P ) ### P = 0.0004 (vs. Ctrl BZD ), ** P = 0.0010 (vs. M1-KI sham ), ## P = 0.0072 (vs. MI-KI BZD ); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). .
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    ( A ) Schematic illustrating the experimental paradigm. Adult male control and Mdga1 Y636C/E751Q KI mice were administered <t>bazedoxifene</t> (BZD; 4.1 mg/kg, intraperitoneally) or vehicle (sham). Six hours post-treatment, the mice were subjected to biochemical, electrophysiological, and behavioral analyses. ( B , C ) Semi-quantitative immunoblotting of hippocampal synaptic proteins, including Nlgn2, GABA A receptor subunit, VGAT, and gephyrin from BZD- or sham-treated mice. β-actin was used as a loading control for normalization. Quantification of normalized protein levels ( C ) revealed that BZD rescued the enhanced expression of synaptic proteins observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 6 per group; (Nlgn2) * P = 0.0220, # P = 0.0313; (GABA A Rγ2) ** P = 0.0021, # P = 0.0495; (VGAT) ** P = 0.0059, # P = 0.0343; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( D , E ) Representative immunoblots ( D ) and quantification ( E ) of phosphorylated SynI, SynIIa, and SynIIb proteins obtained via immunoprecipitation with anti-phospho-serine antibody and normalized to total Syn levels. BZD significantly restored phospho-SynII levels in KI hippocampi. Data are means ± SEMs ( n = 4 independent experiments; (SynIIa) **P = 0.0010, ## P = 0.0019; (SynIIb) # P = 0.0441; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( F , G ) ASRs ( F ) and PPI of ASR ( G ) in adult male control and Mdga1 Y636C/E751Q mice given BZD or sham treatment. BZD treatment reversed the reduced ASR in Mdga1 Y636C/E751Q KI mice, but failed to rescue the deficits in PPI. Data are presented as means ± SEMs ( n = 20–21 mice/group; ( F ) * P = 0.0444 (115 dB), * P = 0.0281 (120 dB), # P = 0.0344 (120 dB); ( G ) * P = 0.0195 (73 dB), * P = 0.0205 (76 dB), * P = 0.0429 (79 dB); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( H – K ) USVs recorded from socially isolated adult male mice. Representative traces are shown in ( H ). BZD treatment normalized the increased number of USV calls ( I ) observed in Mdga1 Y636C/E751Q KI mice. Call length ( J ) was not significantly altered across groups. The altered distribution of call types in Mdga1 Y636C/E751Q KI mice was also partially rescued by BZD, including restoration of the reduced proportion of complex trill calls ( K ). Data are means ± SEMs ( n = 9–10 mice/group; ( I ) * P = 0.0323, # P = 0.0456; ( K ) ** P = 0.0089, ## P = 0.0045; # indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( L – P ) Electrophysiological recordings of dendritic eIPSCs in CA1 pyramidal neurons at P56. Representative traces ( L , O ) and quantification of I–O responses ( M , N ) and paired-pulse ratio (PPR; P ) revealed that BZD rescued the increased inhibitory input strength and the presynaptic release probability abnormalities observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 14–21 cells/group; ( M ) (30 μA) ** P = 0.0065 (vs. MI-KI Sham ), ## P = 0.0064 (vs. MI-KI BZD ); (40 μA) ### P = 0.0003 (vs. Ctrl BZD ), *** P = 0.0001 (vs. MI-KI Sham ), ### P = 0.0004 (vs. MI-KI BZD ); (50 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); (60 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); ( N ) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. M1-KI sham ); ( P ) ### P = 0.0004 (vs. Ctrl BZD ), ** P = 0.0010 (vs. M1-KI sham ), ## P = 0.0072 (vs. MI-KI BZD ); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). .
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    Effects of <t>bazedoxifene,</t> abemaciclib and their combination on cell viability. Co-treatment with bazeboxifene and abemaciclib in (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells exhibited a synergistic effect, and inhibited cell viability more significantly than either drug monotherapy or DMSO. Data are presented as the mean ± standard deviation. **P<0.01, ***P<0.001, ****P<0.0001. CI<1 indicates a synergistic effect, CI>1 indicates an antagonistic effect and CI=1 indicates an additive effect. Ac, abemaciclib; Ac0.25, 0.25 µM Ac; Ac0.5, 0.5 µM Ac; Bz, bazedoxifene; Bz0.5, 0.5 µM Bz; Bz5, 5 µM Bz; CI, combination index; ns, not significant.
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    Image Search Results


    a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or bazedoxifene acetate (BZA) ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Mitochondrial vulnerability underlies myocarditis from COVID-19 mRNA vaccine

    doi: 10.1038/s41467-026-71295-1

    Figure Lengend Snippet: a – c LVEF was measured at 0 and 5 days post-administration of mRNA-1273 in Polg +/D257A mice treated with vehicle ( a ; n = 6), testosterone enanthate (TTE) ( b ; n = 5), or bazedoxifene acetate (BZA) ( c ; n = 6). n represents biologically independent mice. All experiments were performed using male mice aged 8–10 weeks. The centre line indicates the median, the box limits indicate IQR (25th-75th percentiles), and the whiskers extend to 1.5 x IQR ( a – c ). Two-tailed, paired Student’s t -test ( a – c ). Source data are provided as a Source Data file.

    Article Snippet: Mice were also intraperitoneally treated with 3 mg/kg bazedoxifene acetate (BZA) (MedchemExpress) or 10 mg/kg testosterone enanthate (TTE) (Fujifilm) dissolved in 100 μl of corn oil, and 1 mg/kg GSK'074 (MedchemExpress), 2 mg/kg MitoQ (Selleck) dissolved in 100 μl of 10% methylcellulose (Fujifilm) containing 0.01% tween-80 (Nacalai).

    Techniques: Two Tailed Test

    ( A ) Schematic illustrating the experimental paradigm. Adult male control and Mdga1 Y636C/E751Q KI mice were administered bazedoxifene (BZD; 4.1 mg/kg, intraperitoneally) or vehicle (sham). Six hours post-treatment, the mice were subjected to biochemical, electrophysiological, and behavioral analyses. ( B , C ) Semi-quantitative immunoblotting of hippocampal synaptic proteins, including Nlgn2, GABA A receptor subunit, VGAT, and gephyrin from BZD- or sham-treated mice. β-actin was used as a loading control for normalization. Quantification of normalized protein levels ( C ) revealed that BZD rescued the enhanced expression of synaptic proteins observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 6 per group; (Nlgn2) * P = 0.0220, # P = 0.0313; (GABA A Rγ2) ** P = 0.0021, # P = 0.0495; (VGAT) ** P = 0.0059, # P = 0.0343; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( D , E ) Representative immunoblots ( D ) and quantification ( E ) of phosphorylated SynI, SynIIa, and SynIIb proteins obtained via immunoprecipitation with anti-phospho-serine antibody and normalized to total Syn levels. BZD significantly restored phospho-SynII levels in KI hippocampi. Data are means ± SEMs ( n = 4 independent experiments; (SynIIa) **P = 0.0010, ## P = 0.0019; (SynIIb) # P = 0.0441; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( F , G ) ASRs ( F ) and PPI of ASR ( G ) in adult male control and Mdga1 Y636C/E751Q mice given BZD or sham treatment. BZD treatment reversed the reduced ASR in Mdga1 Y636C/E751Q KI mice, but failed to rescue the deficits in PPI. Data are presented as means ± SEMs ( n = 20–21 mice/group; ( F ) * P = 0.0444 (115 dB), * P = 0.0281 (120 dB), # P = 0.0344 (120 dB); ( G ) * P = 0.0195 (73 dB), * P = 0.0205 (76 dB), * P = 0.0429 (79 dB); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( H – K ) USVs recorded from socially isolated adult male mice. Representative traces are shown in ( H ). BZD treatment normalized the increased number of USV calls ( I ) observed in Mdga1 Y636C/E751Q KI mice. Call length ( J ) was not significantly altered across groups. The altered distribution of call types in Mdga1 Y636C/E751Q KI mice was also partially rescued by BZD, including restoration of the reduced proportion of complex trill calls ( K ). Data are means ± SEMs ( n = 9–10 mice/group; ( I ) * P = 0.0323, # P = 0.0456; ( K ) ** P = 0.0089, ## P = 0.0045; # indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( L – P ) Electrophysiological recordings of dendritic eIPSCs in CA1 pyramidal neurons at P56. Representative traces ( L , O ) and quantification of I–O responses ( M , N ) and paired-pulse ratio (PPR; P ) revealed that BZD rescued the increased inhibitory input strength and the presynaptic release probability abnormalities observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 14–21 cells/group; ( M ) (30 μA) ** P = 0.0065 (vs. MI-KI Sham ), ## P = 0.0064 (vs. MI-KI BZD ); (40 μA) ### P = 0.0003 (vs. Ctrl BZD ), *** P = 0.0001 (vs. MI-KI Sham ), ### P = 0.0004 (vs. MI-KI BZD ); (50 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); (60 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); ( N ) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. M1-KI sham ); ( P ) ### P = 0.0004 (vs. Ctrl BZD ), ** P = 0.0010 (vs. M1-KI sham ), ## P = 0.0072 (vs. MI-KI BZD ); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). .

    Journal: EMBO Molecular Medicine

    Article Title: Bazedoxifene reverses sexually dimorphic autistic-like abnormalities in biallelic MDGA1-mutant mice

    doi: 10.1038/s44321-026-00402-y

    Figure Lengend Snippet: ( A ) Schematic illustrating the experimental paradigm. Adult male control and Mdga1 Y636C/E751Q KI mice were administered bazedoxifene (BZD; 4.1 mg/kg, intraperitoneally) or vehicle (sham). Six hours post-treatment, the mice were subjected to biochemical, electrophysiological, and behavioral analyses. ( B , C ) Semi-quantitative immunoblotting of hippocampal synaptic proteins, including Nlgn2, GABA A receptor subunit, VGAT, and gephyrin from BZD- or sham-treated mice. β-actin was used as a loading control for normalization. Quantification of normalized protein levels ( C ) revealed that BZD rescued the enhanced expression of synaptic proteins observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 6 per group; (Nlgn2) * P = 0.0220, # P = 0.0313; (GABA A Rγ2) ** P = 0.0021, # P = 0.0495; (VGAT) ** P = 0.0059, # P = 0.0343; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( D , E ) Representative immunoblots ( D ) and quantification ( E ) of phosphorylated SynI, SynIIa, and SynIIb proteins obtained via immunoprecipitation with anti-phospho-serine antibody and normalized to total Syn levels. BZD significantly restored phospho-SynII levels in KI hippocampi. Data are means ± SEMs ( n = 4 independent experiments; (SynIIa) **P = 0.0010, ## P = 0.0019; (SynIIb) # P = 0.0441; ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA with Tukey’s post hoc test). ( F , G ) ASRs ( F ) and PPI of ASR ( G ) in adult male control and Mdga1 Y636C/E751Q mice given BZD or sham treatment. BZD treatment reversed the reduced ASR in Mdga1 Y636C/E751Q KI mice, but failed to rescue the deficits in PPI. Data are presented as means ± SEMs ( n = 20–21 mice/group; ( F ) * P = 0.0444 (115 dB), * P = 0.0281 (120 dB), # P = 0.0344 (120 dB); ( G ) * P = 0.0195 (73 dB), * P = 0.0205 (76 dB), * P = 0.0429 (79 dB); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( H – K ) USVs recorded from socially isolated adult male mice. Representative traces are shown in ( H ). BZD treatment normalized the increased number of USV calls ( I ) observed in Mdga1 Y636C/E751Q KI mice. Call length ( J ) was not significantly altered across groups. The altered distribution of call types in Mdga1 Y636C/E751Q KI mice was also partially rescued by BZD, including restoration of the reduced proportion of complex trill calls ( K ). Data are means ± SEMs ( n = 9–10 mice/group; ( I ) * P = 0.0323, # P = 0.0456; ( K ) ** P = 0.0089, ## P = 0.0045; # indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). ( L – P ) Electrophysiological recordings of dendritic eIPSCs in CA1 pyramidal neurons at P56. Representative traces ( L , O ) and quantification of I–O responses ( M , N ) and paired-pulse ratio (PPR; P ) revealed that BZD rescued the increased inhibitory input strength and the presynaptic release probability abnormalities observed in Mdga1 Y636C/E751Q KI mice. Data are means ± SEMs ( n = 14–21 cells/group; ( M ) (30 μA) ** P = 0.0065 (vs. MI-KI Sham ), ## P = 0.0064 (vs. MI-KI BZD ); (40 μA) ### P = 0.0003 (vs. Ctrl BZD ), *** P = 0.0001 (vs. MI-KI Sham ), ### P = 0.0004 (vs. MI-KI BZD ); (50 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); (60 μA) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. MI-KI Sham ), #### P < 0.0001 (vs. MI-KI BZD ); ( N ) #### P < 0.0001 (vs. Ctrl BZD ), **** P < 0.0001 (vs. M1-KI sham ); ( P ) ### P = 0.0004 (vs. Ctrl BZD ), ** P = 0.0010 (vs. M1-KI sham ), ## P = 0.0072 (vs. MI-KI BZD ); ‘#’ indicates statistical comparisons with their counterparts; two-way ANOVA followed by Tukey’s post hoc test). .

    Article Snippet: The following drugs were commercially purchased: Bazedoxifene acetate (Cat# HY-A0036) and Fulvestrant (Cat# HY-13636) from MedChemExpress (MCE); CNQX (Cat# 0190), D-AP5 (Cat# 0106) and picrotoxin (Cat# 1128) from Tocris Bioscience; Tetrodotoxin (TTX; Cat# 14964) from Cayman Chemical; and 2,2,2-tribromoethyl alcohol (Cat# T48402 ) from Sigma-Aldrich.

    Techniques: Control, Western Blot, Expressing, Immunoprecipitation, Isolation

    Effects of bazedoxifene, abemaciclib and their combination on cell viability. Co-treatment with bazeboxifene and abemaciclib in (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells exhibited a synergistic effect, and inhibited cell viability more significantly than either drug monotherapy or DMSO. Data are presented as the mean ± standard deviation. **P<0.01, ***P<0.001, ****P<0.0001. CI<1 indicates a synergistic effect, CI>1 indicates an antagonistic effect and CI=1 indicates an additive effect. Ac, abemaciclib; Ac0.25, 0.25 µM Ac; Ac0.5, 0.5 µM Ac; Bz, bazedoxifene; Bz0.5, 0.5 µM Bz; Bz5, 5 µM Bz; CI, combination index; ns, not significant.

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on cell viability. Co-treatment with bazeboxifene and abemaciclib in (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells exhibited a synergistic effect, and inhibited cell viability more significantly than either drug monotherapy or DMSO. Data are presented as the mean ± standard deviation. **P<0.01, ***P<0.001, ****P<0.0001. CI<1 indicates a synergistic effect, CI>1 indicates an antagonistic effect and CI=1 indicates an additive effect. Ac, abemaciclib; Ac0.25, 0.25 µM Ac; Ac0.5, 0.5 µM Ac; Bz, bazedoxifene; Bz0.5, 0.5 µM Bz; Bz5, 5 µM Bz; CI, combination index; ns, not significant.

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: Standard Deviation

    Effects of bazedoxifene, abemaciclib and their combination on IL-6/STAT3 signaling and downstream targets. Western blot analysis of pSTAT3, STAT3, cyclin D1 and GAPDH after treatment with DMSO, bazedoxifene, abemaciclib or bazedoxifene plus abemaciclib in (A) SUM159 and (B) MDA-MB-231 cells. Abemaciclib monotherapy induced pSTAT3 and cyclin D1, while the bazedoxifene plus abemaciclib combination combated this induction. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz; p, phosphorylated.

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on IL-6/STAT3 signaling and downstream targets. Western blot analysis of pSTAT3, STAT3, cyclin D1 and GAPDH after treatment with DMSO, bazedoxifene, abemaciclib or bazedoxifene plus abemaciclib in (A) SUM159 and (B) MDA-MB-231 cells. Abemaciclib monotherapy induced pSTAT3 and cyclin D1, while the bazedoxifene plus abemaciclib combination combated this induction. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz; p, phosphorylated.

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: Western Blot

    Effects of bazedoxifene, abemaciclib and their combination on cell cycle progression. Cell cycle analysis of (A) SUM159 cells, including (B) quantification, and (C) MDA-MB-231 cells, including (D) quantification, after treatment with DMSO, bazedoxifene, abemaciclib or the bazedoxifene plus abemaciclib combination. The strongest G 0 /G 1 blockage was induced by the bazedoxifene plus abemaciclib combination. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz.

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on cell cycle progression. Cell cycle analysis of (A) SUM159 cells, including (B) quantification, and (C) MDA-MB-231 cells, including (D) quantification, after treatment with DMSO, bazedoxifene, abemaciclib or the bazedoxifene plus abemaciclib combination. The strongest G 0 /G 1 blockage was induced by the bazedoxifene plus abemaciclib combination. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz.

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: Cell Cycle Assay

    Effects of bazedoxifene, abemaciclib and their combination on cell migration. The migration of (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells was inhibited to a greater extent when cells were treated with bazedoxifene plus abemaciclib compared with either monotherapy or DMSO. Images were captured at a magnification of ×10. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. Ac, abemaciclib; Ac1, 1 µM Ac; Ac2, 2 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz.

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on cell migration. The migration of (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells was inhibited to a greater extent when cells were treated with bazedoxifene plus abemaciclib compared with either monotherapy or DMSO. Images were captured at a magnification of ×10. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. Ac, abemaciclib; Ac1, 1 µM Ac; Ac2, 2 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz; Bz10, 10 µM Bz.

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: Migration, Standard Deviation

    Effects of bazedoxifene, abemaciclib and their combination on cell invasion. The invasion of (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells was inhibited to a greater extent when cells were treated with bazedoxifene plus abemaciclib, compared with either monotherapy or DMSO. Images were captured at a magnification of ×10. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. Ac, abemaciclib; Ac0.25, 0.25 µM Ac; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz.

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on cell invasion. The invasion of (A) SUM159, (B) MDA-MB-231 and (C) 4T1 cells was inhibited to a greater extent when cells were treated with bazedoxifene plus abemaciclib, compared with either monotherapy or DMSO. Images were captured at a magnification of ×10. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. Ac, abemaciclib; Ac0.25, 0.25 µM Ac; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz5, 5 µM Bz.

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: Standard Deviation

    Effects of bazedoxifene, abemaciclib and their combination on apoptosis. Apoptosis analysis of (A) MDA-MB-231 cells after treatment with DMSO, bazedoxifene, abemaciclib, or the bazedoxifene plus abemaciclib combination, and (B) its quantification. The greatest induction of apoptosis was achieved by the bazedoxifene plus abemaciclib combination compared with either monotherapy or DMSO treatment. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz10, 10 µM Bz; DN, double negative (negative for FITC and PI, indicative of live cells); FITC_positive, only positive for FITC (indicative of cells in early apoptosis); DP, double positive (positive for FITC and PI, indicative of cells in late apoptosis); PI_positive, only positive for PI (indicative of dead cells).

    Journal: Oncology Letters

    Article Title: Synergistic effect of bazedoxifene and abemaciclib co‑treatment in triple‑negative breast cancer cells in vitro

    doi: 10.3892/ol.2024.14688

    Figure Lengend Snippet: Effects of bazedoxifene, abemaciclib and their combination on apoptosis. Apoptosis analysis of (A) MDA-MB-231 cells after treatment with DMSO, bazedoxifene, abemaciclib, or the bazedoxifene plus abemaciclib combination, and (B) its quantification. The greatest induction of apoptosis was achieved by the bazedoxifene plus abemaciclib combination compared with either monotherapy or DMSO treatment. Ac, abemaciclib; Ac1, 1 µM Ac; Bz, bazedoxifene; Bz10, 10 µM Bz; DN, double negative (negative for FITC and PI, indicative of live cells); FITC_positive, only positive for FITC (indicative of cells in early apoptosis); DP, double positive (positive for FITC and PI, indicative of cells in late apoptosis); PI_positive, only positive for PI (indicative of dead cells).

    Article Snippet: Bazedoxifene acetate (cat. no. 102233) and abemaciclib mesylate (cat. no. 206973) were purchased from MedKoo Biosciences, Inc.

    Techniques: