dimethyl sulfoxide Search Results


dimethyl sulfoxide  (MedChemExpress)
96
MedChemExpress dimethyl sulfoxide
Dimethyl Sulfoxide, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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dimethyl sulfoxide  (MuseChem Chemicals)
91
MuseChem Chemicals dimethyl sulfoxide
Dimethyl Sulfoxide, supplied by MuseChem Chemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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dmso  (Santa Cruz Biotechnology)
94
Santa Cruz Biotechnology dmso
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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dimethyl sulfoxide  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology dimethyl sulfoxide
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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dimethyl sulfoxide  (Toronto Research Chemicals)
91
Toronto Research Chemicals dimethyl sulfoxide
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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solvent control  (Biosynth Carbosynth)
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Biosynth Carbosynth solvent control
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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dmso  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc dmso
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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sterile dimethyl sulfoxide dmso  (MedChemExpress)
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MedChemExpress sterile dimethyl sulfoxide dmso
HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and <t>DMSO</t> (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without <t>(−Baf.A1)</t> <t>Bafilomycin</t> A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.
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dmso  (MedChemExpress)
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MedChemExpress dmso
a Cellchat analyzed cell interaction patterns in CRC tissues. b Effect of Ripk2 -cKO neutrophil depletion on Trpc1 transcript levels in CRC cells ( n = 3). TRPC1 protein levels in CRC cells ( n = 4) after anti-Ly6G antibody ( c ) <t>or</t> <t>PMA/DNase</t> I ( d ) injections. For d , P values compared PMA~NETs vs. <t>DMSO~NETs</t> and Dnase I~NETs vs. DMSO~NETs. e Calcium levels in CRC cells ( n = 3). f Pathways affected by Ripk2 -cKO neutrophil depletion in CRC cells. Neutrophil depletion ( g ), Trpc1 -KO ( h ), neutrophil depletion with Trpc1 -OE ( i ), or PMA-stimulated NETs with Trpc1 -KO ( j ) effects on p-STAT3/STAT3 levels in CRC cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. Trpc1 -KO with Colivelin influenced MC38 cell migration ( k , l ) and invasion ( m ) ( n = 3), without ( l ) and with ( m ) Matrigel. n Interaction analysis of S100A8 and S100A9 in MC38 cells ( n = 3). o Trpc1 -KO effects on S100A8-S100A9 interaction in MC38 cells ( n = 3). p S100A8 and S100A9 docking model. q Impact of S100A8-4A and S100A9-3A on their interaction in MC38 cells ( n = 3). r Trpc1 -OE or S100A8/9-7A effects on MC38 cell migration ( n = 3). Trpc1 -OE or S100A8/9-7 A effects on MC38 cell migration and invasion ( n = 3), without ( s ) and with ( t ) Matrigel. u PMA-stimulated NETs or S100A8/9-7A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for p-STAT3 and GAPDH-p, and an additional one for STAT3 and GAPDH-T. v Trpc1 -OE or S100A8/9-7 A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. w S100a8/9 -KO or Colivelin effects on MC38 cell migration ( n = 3). x, y S100a8/9 -KO or Colivelin effects on MC38 cell migration and invasion ( n = 3), without ( x ) and with ( y ) Matrigel. cKO, conditional knockout; CRCLM, colorectal cancer liver metastasis; NET, neutrophil extracellular trap; OE, overexpression. n represented the number of independent biological repetitions. Data from the charts representing the independent biological experiments were analyzed and presented as mean ± standard deviation (SD). Two-tailed Student’s T-test ( b – d , g – k , m , r , s , x ), two-tailed Wilcoxon test ( e , f , l , t – w , y ). Significance: * P < 0.05; ** P < 0.01; *** P < 0.001. Source data and exact P values are provided as a Source Data file.
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dimethyl sulfoxide d6  (Biosynth Carbosynth)
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a Cellchat analyzed cell interaction patterns in CRC tissues. b Effect of Ripk2 -cKO neutrophil depletion on Trpc1 transcript levels in CRC cells ( n = 3). TRPC1 protein levels in CRC cells ( n = 4) after anti-Ly6G antibody ( c ) <t>or</t> <t>PMA/DNase</t> I ( d ) injections. For d , P values compared PMA~NETs vs. <t>DMSO~NETs</t> and Dnase I~NETs vs. DMSO~NETs. e Calcium levels in CRC cells ( n = 3). f Pathways affected by Ripk2 -cKO neutrophil depletion in CRC cells. Neutrophil depletion ( g ), Trpc1 -KO ( h ), neutrophil depletion with Trpc1 -OE ( i ), or PMA-stimulated NETs with Trpc1 -KO ( j ) effects on p-STAT3/STAT3 levels in CRC cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. Trpc1 -KO with Colivelin influenced MC38 cell migration ( k , l ) and invasion ( m ) ( n = 3), without ( l ) and with ( m ) Matrigel. n Interaction analysis of S100A8 and S100A9 in MC38 cells ( n = 3). o Trpc1 -KO effects on S100A8-S100A9 interaction in MC38 cells ( n = 3). p S100A8 and S100A9 docking model. q Impact of S100A8-4A and S100A9-3A on their interaction in MC38 cells ( n = 3). r Trpc1 -OE or S100A8/9-7A effects on MC38 cell migration ( n = 3). Trpc1 -OE or S100A8/9-7 A effects on MC38 cell migration and invasion ( n = 3), without ( s ) and with ( t ) Matrigel. u PMA-stimulated NETs or S100A8/9-7A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for p-STAT3 and GAPDH-p, and an additional one for STAT3 and GAPDH-T. v Trpc1 -OE or S100A8/9-7 A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. w S100a8/9 -KO or Colivelin effects on MC38 cell migration ( n = 3). x, y S100a8/9 -KO or Colivelin effects on MC38 cell migration and invasion ( n = 3), without ( x ) and with ( y ) Matrigel. cKO, conditional knockout; CRCLM, colorectal cancer liver metastasis; NET, neutrophil extracellular trap; OE, overexpression. n represented the number of independent biological repetitions. Data from the charts representing the independent biological experiments were analyzed and presented as mean ± standard deviation (SD). Two-tailed Student’s T-test ( b – d , g – k , m , r , s , x ), two-tailed Wilcoxon test ( e , f , l , t – w , y ). Significance: * P < 0.05; ** P < 0.01; *** P < 0.001. Source data and exact P values are provided as a Source Data file.
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promethazine sulfoxide  (Toronto Research Chemicals)
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Toronto Research Chemicals promethazine sulfoxide
Chemical structure of (a) <t>promethazine</t> hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.
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nacch in dmso  (BOC Sciences)
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Chemical structure of (a) <t>promethazine</t> hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.
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HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and DMSO (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without (−Baf.A1) Bafilomycin A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.

Journal: Journal of Innate Immunity

Article Title: The Novel Inducer of Innate Immunity HO53 Stimulates Autophagy in Human Airway Epithelial Cells

doi: 10.1159/000521602

Figure Lengend Snippet: HO53 treatment induces autophagy in human airway epithelial cells. BCi cells were stimulated for 24 h with different doses of HO53, and 250 nM Rapa was used as a positive control for autophagy induction, and DMSO (final concentration of 0.3%) was used as a solv, all in combination with (+Baf.A1) or without (−Baf.A1) Bafilomycin A1 (100 nM). Treatment of differentiated BCi cells was performed by addition of the compound to the lower chamber of the trans-well insert. Induction of autophagy in the ALI culture ( a ) and undifferentiated BCi ( b ) was evaluated by analysis of LC3B processing on Western blotting. The processing of LC3B-I to LC3B-II was quantified by measurement of the LC3B-II band intensity versus GAPDH loading control and presented as the LC3B-II/GAPDH ratio. Data present average ± SEM from n = 3 independent experiments analyzed by one-way ANOVA with Sidak post hoc test, where * p < 0.05, ** p < 0.01 and ns versus solvent control, & p < 0.05 versus 50 μM HO53, && p < 0.01 versus 12.5 μM HO53. Samples were run in one experiment on separate gels/blots processed in parallel, and full-length blots are presented in Supplementary Figure S7. c Analysis of the autophagy induction by HO53 (75 μM) in ALI-cultured BCi cells by immunostaining of LC3B puncta (green), nuclei (blue), and occludin (red), a tight-junction protein characteristic for the differentiated BCi cells in the ALI culture. The scale bar is 10 μm. Autophagy flux in ALI-cultured BCi was calculated based on number of LC3B+ (positive) puncta using the formula: ( sample + Baf.A1 )/ sample presented as autophagy flux LC3B + puncta. Data present average ± SEM from n = 5 independent experiments analyzed by an unpaired t -test, where * p < 0.05. d TEM analysis of differentiated BCi cells treated with HO53 (75 μM) and Bafilomycin A1 (100 nm) for 24 h. Autophagosomes are indicated by red arrows. TF indicates the trans-well filter/insert; red squares indicate a magnified area with scale bars for images as indicated (from left to right) 2 μm, 1 μm and 200 nm. Representative images of n = 4 trans-well inserts from 2 independent experiments. ns, nonsignificant; solv, solvent control; Rapa, rapamycin; SEM, standard error of mean.

Article Snippet: UltroserG (15950-017) was obtained from Pall Life Sciences and DMSO (sc-358801), Bafilomycin A1 (sc-201550), and rapamycin (sc-3504) from Santa Cruz.

Techniques: Positive Control, Concentration Assay, Western Blot, Control, Solvent, Cell Culture, Immunostaining

a Cellchat analyzed cell interaction patterns in CRC tissues. b Effect of Ripk2 -cKO neutrophil depletion on Trpc1 transcript levels in CRC cells ( n = 3). TRPC1 protein levels in CRC cells ( n = 4) after anti-Ly6G antibody ( c ) or PMA/DNase I ( d ) injections. For d , P values compared PMA~NETs vs. DMSO~NETs and Dnase I~NETs vs. DMSO~NETs. e Calcium levels in CRC cells ( n = 3). f Pathways affected by Ripk2 -cKO neutrophil depletion in CRC cells. Neutrophil depletion ( g ), Trpc1 -KO ( h ), neutrophil depletion with Trpc1 -OE ( i ), or PMA-stimulated NETs with Trpc1 -KO ( j ) effects on p-STAT3/STAT3 levels in CRC cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. Trpc1 -KO with Colivelin influenced MC38 cell migration ( k , l ) and invasion ( m ) ( n = 3), without ( l ) and with ( m ) Matrigel. n Interaction analysis of S100A8 and S100A9 in MC38 cells ( n = 3). o Trpc1 -KO effects on S100A8-S100A9 interaction in MC38 cells ( n = 3). p S100A8 and S100A9 docking model. q Impact of S100A8-4A and S100A9-3A on their interaction in MC38 cells ( n = 3). r Trpc1 -OE or S100A8/9-7A effects on MC38 cell migration ( n = 3). Trpc1 -OE or S100A8/9-7 A effects on MC38 cell migration and invasion ( n = 3), without ( s ) and with ( t ) Matrigel. u PMA-stimulated NETs or S100A8/9-7A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for p-STAT3 and GAPDH-p, and an additional one for STAT3 and GAPDH-T. v Trpc1 -OE or S100A8/9-7 A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. w S100a8/9 -KO or Colivelin effects on MC38 cell migration ( n = 3). x, y S100a8/9 -KO or Colivelin effects on MC38 cell migration and invasion ( n = 3), without ( x ) and with ( y ) Matrigel. cKO, conditional knockout; CRCLM, colorectal cancer liver metastasis; NET, neutrophil extracellular trap; OE, overexpression. n represented the number of independent biological repetitions. Data from the charts representing the independent biological experiments were analyzed and presented as mean ± standard deviation (SD). Two-tailed Student’s T-test ( b – d , g – k , m , r , s , x ), two-tailed Wilcoxon test ( e , f , l , t – w , y ). Significance: * P < 0.05; ** P < 0.01; *** P < 0.001. Source data and exact P values are provided as a Source Data file.

Journal: Nature Communications

Article Title: Escherichia coli promotes colorectal cancer metastasis by maintaining enhancer-promoter loops through releasing neutrophil extracellular traps

doi: 10.1038/s41467-026-69005-y

Figure Lengend Snippet: a Cellchat analyzed cell interaction patterns in CRC tissues. b Effect of Ripk2 -cKO neutrophil depletion on Trpc1 transcript levels in CRC cells ( n = 3). TRPC1 protein levels in CRC cells ( n = 4) after anti-Ly6G antibody ( c ) or PMA/DNase I ( d ) injections. For d , P values compared PMA~NETs vs. DMSO~NETs and Dnase I~NETs vs. DMSO~NETs. e Calcium levels in CRC cells ( n = 3). f Pathways affected by Ripk2 -cKO neutrophil depletion in CRC cells. Neutrophil depletion ( g ), Trpc1 -KO ( h ), neutrophil depletion with Trpc1 -OE ( i ), or PMA-stimulated NETs with Trpc1 -KO ( j ) effects on p-STAT3/STAT3 levels in CRC cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. Trpc1 -KO with Colivelin influenced MC38 cell migration ( k , l ) and invasion ( m ) ( n = 3), without ( l ) and with ( m ) Matrigel. n Interaction analysis of S100A8 and S100A9 in MC38 cells ( n = 3). o Trpc1 -KO effects on S100A8-S100A9 interaction in MC38 cells ( n = 3). p S100A8 and S100A9 docking model. q Impact of S100A8-4A and S100A9-3A on their interaction in MC38 cells ( n = 3). r Trpc1 -OE or S100A8/9-7A effects on MC38 cell migration ( n = 3). Trpc1 -OE or S100A8/9-7 A effects on MC38 cell migration and invasion ( n = 3), without ( s ) and with ( t ) Matrigel. u PMA-stimulated NETs or S100A8/9-7A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for p-STAT3 and GAPDH-p, and an additional one for STAT3 and GAPDH-T. v Trpc1 -OE or S100A8/9-7 A effects on p-STAT3/STAT3 levels in MC38 cells ( n = 3). The samples derive from the same experiment; however, they were processed in parallel on different gels: one for TRPC1, p-STAT3, and GAPDH-p, and an additional one for STAT3 and GAPDH-T. w S100a8/9 -KO or Colivelin effects on MC38 cell migration ( n = 3). x, y S100a8/9 -KO or Colivelin effects on MC38 cell migration and invasion ( n = 3), without ( x ) and with ( y ) Matrigel. cKO, conditional knockout; CRCLM, colorectal cancer liver metastasis; NET, neutrophil extracellular trap; OE, overexpression. n represented the number of independent biological repetitions. Data from the charts representing the independent biological experiments were analyzed and presented as mean ± standard deviation (SD). Two-tailed Student’s T-test ( b – d , g – k , m , r , s , x ), two-tailed Wilcoxon test ( e , f , l , t – w , y ). Significance: * P < 0.05; ** P < 0.01; *** P < 0.001. Source data and exact P values are provided as a Source Data file.

Article Snippet: 3 d after the injection of MC38 cells or patient organoids, Anti-CD3 Antibody (OKT-3) (3 mg/kg, HY-P990864, MedChemExpress, NJ, USA), Anumigilimab (2 mg/kg, HY-P99440, MedChemExpress), Ca 2+ channel agonist 1 (4 mg/kg, HY-41076, MedChemExpress), Clodronate Liposomes (40337ES08, Yeasen, China), DMSO (HY-Y0320C, MedChemExpress), DNase I (10 mg/kg, 10104159001, Merck), GSK484 hydrochloride (4 mg/kg, HY-100514, MedChemExpress), GSK583 (4 mg/kg, HY-100339, MedChemExpress), InVivoMAb anti-mouse CD3ε (5 mg/kg, catalog number: BE0001-1, clone name: 145-2C11, Bio X Cell, PA, USA), InVivoMAb anti-mouse Ly6G (5 mg/kg, catalog number: BE0075, clone name: RB6-8C5, Bio X Cell), InVivoMAb rat IgG2a isotype control (5 mg/kg, catalog number: BE0251, clone name: RG7/1.30, Bio X Cell), JNK-IN-8 (3 mg/kg, HY-13319, MedChemExpress), JSH-23 (5 mg/kg, HY-13982, MedChemExpress), MLKL-IN-1 (5 mg/kg, HY-139878, MedChemExpress), NOD1/2 antagonist-1 (5 mg/kg, HY-146034, MedChemExpress), Paquinimod (5 mg/kg, HY-100442, MedChemExpress), PMA (5 mg/kg, P8139, Merck), p38 MAPK-IN-1 (5 mg/kg, HY-12839, MedChemExpress), SCH772984 (3 mg/kg, HY-50846, MedChemExpress), Sparstolonin B (5 mg/kg, HY-116213, MedChemExpress), or Stattic (5 mg/kg, HY-13818, MedChemExpress) were injected into the tail vein of mice once every three days for a total of five times.

Techniques: Migration, Knock-Out, Over Expression, Standard Deviation, Two Tailed Test

Chemical structure of (a) promethazine hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Chemical structure of (a) promethazine hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques:

MRM transitions, retention time, and conditions of analytes and internal standards.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: MRM transitions, retention time, and conditions of analytes and internal standards.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques:

MS scans for (a) promethazine hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: MS scans for (a) promethazine hydrochloride, (b) PMZSO, (c) schisandrin, (d) metronidazole, and (e) bifendate.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques:

Regression equations, linear ranges, and LLOQs of the three compounds.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Regression equations, linear ranges, and LLOQs of the three compounds.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques:

Intra- and interday precision (RSD, %) and accuracy (bias, %) of QC samples.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Intra- and interday precision (RSD, %) and accuracy (bias, %) of QC samples.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques: Concentration Assay

Recovery and matrix effect of the three analytes in rat plasma.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Recovery and matrix effect of the three analytes in rat plasma.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques: Clinical Proteomics, Concentration Assay

Stability of the analytes in rat plasma under different storage conditions.

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Stability of the analytes in rat plasma under different storage conditions.

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques: Clinical Proteomics, Concentration Assay

Pharmacokinetic parameters of PMZ and PMZSO in rats after oral administration of PMZ with or without S. chinensis ( n = 6-7).

Journal: International Journal of Analytical Chemistry

Article Title: Simultaneous Determination of Schisandrin and Promethazine with Its Metabolite in Rat Plasma by HPLC-MS/MS and Its Application to a Pharmacokinetic Study

doi: 10.1155/2019/3497045

Figure Lengend Snippet: Pharmacokinetic parameters of PMZ and PMZSO in rats after oral administration of PMZ with or without S. chinensis ( n = 6-7).

Article Snippet: Promethazine sulfoxide (Batch No. 1-JGC-73-2, purity >98%) was manufactured by Toronto Research Chemicals (Toronto, Canada).

Techniques: