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Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
Sirolimus, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sirolimus eluting resorbable magnesium scaffold system (dreams 3g rms  (Biotronik GmbH)
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Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
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sirolimus eluting resorbable magnesium scaffold system (dreams 3g rms - by Bioz Stars, 2026-09
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orsiro sirolimus-eluting coronary stent system  (Biotronik GmbH)
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Biotronik GmbH orsiro sirolimus-eluting coronary stent system
Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
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orsiro sirolimus-eluting coronary stent system - by Bioz Stars, 2026-09
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sirolimus-eluting stents (bp-ses  (Biotronik GmbH)
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Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
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sirolimus-eluting stents (bp-ses - by Bioz Stars, 2026-09
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orsiro des (sirolimus-eluting stent  (Biotronik GmbH)
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Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
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orsiro des (sirolimus-eluting stent - by Bioz Stars, 2026-09
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hy 10219  (MedChemExpress)
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MedChemExpress hy 10219
Molecular docking map of WT1 with potential drug targets. (A) WT1 and <t>sirolimus.</t> (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.
Hy 10219, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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autophagy activator rapamycin  (MedChemExpress)
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MedChemExpress autophagy activator rapamycin
Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer <t>Rapamycin</t> (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Autophagy Activator Rapamycin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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autophagy inducer rapamycin  (MedChemExpress)
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MedChemExpress autophagy inducer rapamycin
Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer <t>Rapamycin</t> (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Autophagy Inducer Rapamycin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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autophagy inducer rapamycin - by Bioz Stars, 2026-09
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hy 15979a rapamycin sigma aldrich  (MedChemExpress)
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MedChemExpress hy 15979a rapamycin sigma aldrich
Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer <t>Rapamycin</t> (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Hy 15979a Rapamycin Sigma Aldrich, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sirolimus/H-89+dihydrochloride/pm42532048-297-104-102
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mtor inhibitor rapamycin  (MedChemExpress)
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MedChemExpress mtor inhibitor rapamycin
Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer <t>Rapamycin</t> (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Mtor Inhibitor Rapamycin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sirolimus/Rapamycin/pm42518168-23-27-31
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mtor inhibitor rapamycin - by Bioz Stars, 2026-09
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Image Search Results


Molecular docking map of WT1 with potential drug targets. (A) WT1 and sirolimus. (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.

Journal: Experimental and Therapeutic Medicine

Article Title: Unveiling the comorbidity hub: WT1 drives renal cancer progression in chronic kidney disease and confers sirolimus vulnerability

doi: 10.3892/etm.2026.13214

Figure Lengend Snippet: Molecular docking map of WT1 with potential drug targets. (A) WT1 and sirolimus. (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. (F) WT1 and halofuginone. (G) WT1 and deferoxamine. (H) WT1 and dimethyl sulfoxide. WT1, Wilms tumor 1.

Article Snippet: A dose-response assay was conducted to determine the IC 50 of sirolimus (MedChemExpress) against UOK276 cells using the CCK-8 kit (Dojindo Laboratories, Inc.).

Techniques: Wilms Tumor Assay

Molecular dynamics simulation diagrams. (A) WT1 and sirolimus. (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. WT1, Wilms tumor 1.

Journal: Experimental and Therapeutic Medicine

Article Title: Unveiling the comorbidity hub: WT1 drives renal cancer progression in chronic kidney disease and confers sirolimus vulnerability

doi: 10.3892/etm.2026.13214

Figure Lengend Snippet: Molecular dynamics simulation diagrams. (A) WT1 and sirolimus. (B) WT1 and daunorubicin liposomal. (C) WT1 and tretinoin. (D) WT1 and curcumin. (E) WT1 and cytarabine. WT1, Wilms tumor 1.

Article Snippet: A dose-response assay was conducted to determine the IC 50 of sirolimus (MedChemExpress) against UOK276 cells using the CCK-8 kit (Dojindo Laboratories, Inc.).

Techniques: Wilms Tumor Assay

In vitro antitumor effects of sirolimus in UOK276 renal carcinoma cells. (A) Dose-response curve from the Cell Counting Kit-8 assay used to determine the IC 50 . (B) Bar graph showing the quantification of colony formation, indicating reduced proliferative capacity after sirolimus treatment. (C) Representative images of colony formation assays demonstrating decreased colony number and size following sirolimus exposure. (D) Representative images of Transwell Matrigel invasion assays showing reduced cell invasiveness after sirolimus treatment. (E) Representative fluorescence images of TUNEL staining indicating increased apoptosis following drug exposure. (F) Bar graph quantifying the Transwell invasion assay results, confirming a significant reduction in invaded cells. (G) Bar graph quantifying the TUNEL-positive cells, demonstrating a statistically significant increase in apoptosis. Statistical analysis by one-way ANOVA with Tukey's post hoc test; * P<0.05, ** P<0.01, *** P<0.001. ns, no statistical significance; IC 50 , half-maximal inhibitory concentration; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.

Journal: Experimental and Therapeutic Medicine

Article Title: Unveiling the comorbidity hub: WT1 drives renal cancer progression in chronic kidney disease and confers sirolimus vulnerability

doi: 10.3892/etm.2026.13214

Figure Lengend Snippet: In vitro antitumor effects of sirolimus in UOK276 renal carcinoma cells. (A) Dose-response curve from the Cell Counting Kit-8 assay used to determine the IC 50 . (B) Bar graph showing the quantification of colony formation, indicating reduced proliferative capacity after sirolimus treatment. (C) Representative images of colony formation assays demonstrating decreased colony number and size following sirolimus exposure. (D) Representative images of Transwell Matrigel invasion assays showing reduced cell invasiveness after sirolimus treatment. (E) Representative fluorescence images of TUNEL staining indicating increased apoptosis following drug exposure. (F) Bar graph quantifying the Transwell invasion assay results, confirming a significant reduction in invaded cells. (G) Bar graph quantifying the TUNEL-positive cells, demonstrating a statistically significant increase in apoptosis. Statistical analysis by one-way ANOVA with Tukey's post hoc test; * P<0.05, ** P<0.01, *** P<0.001. ns, no statistical significance; IC 50 , half-maximal inhibitory concentration; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.

Article Snippet: A dose-response assay was conducted to determine the IC 50 of sirolimus (MedChemExpress) against UOK276 cells using the CCK-8 kit (Dojindo Laboratories, Inc.).

Techniques: In Vitro, Cell Counting, Fluorescence, TUNEL Assay, Staining, Transwell Invasion Assay, Concentration Assay

Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer Rapamycin (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: Lipoprotein (a) fuels EV71 replication by activating p38 MAPK-autophagy axis

doi: 10.3389/fimmu.2026.1865808

Figure Lengend Snippet: Modulation of Lp(a)-induced autophagy alters EV71 replication. (A) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor Chloroquine (CQ). Co-treatment with CQ and Lp(a) further decreased LC3-II and VP1 levels compared to EV71 infection alone or with Lp(a). Quantification (bottom) showed that Lp(a) increases LC3-II and VP1 levels during EV71 infection, and CQ decreases LC3-II accumulation and VP1 expression. (B) The combination of EV71, Lp(a), and CQ shows a marked decrease in LC3-positive puncta. (C) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inhibitor 3-Methyladenine (3-MA). 3-MA treatment suppresses Lp(a)-induced LC3-II accumulation and reduced VP1 protein levels. Quantification (bottom) shows significant suppression of Lp(a)-enhanced EV71 replication by 3-MA. (D) 3-MA treatment reduces the formation of LC3-positive puncta induced by EV71 and Lp(a). (E) Cells were treated with 40 mg/L Lp(a) and/or the autophagy inducer Rapamycin (Rapa). Rapamycin enhances the LC3-II accumulation induced by Lp(a) and further increased VP1 protein levels. Quantification (bottom) shows significant upregulation of LC3-II and VP1 following autophagy activation. (F) Rapamycin treatment enhances the formation of LC3-positive puncta induced by EV71 and Lp(a). Cells were stained for LC3 (red) to visualize autophagosomes and with DAPI (blue) for nuclei. Scale bar, 10 µm. Data are presented as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The autophagy inhibitor 3-methyladenine (3-MA) (MCE, MedChemExpress), chloroquine (CQ) (MCE, MedChemExpress) and the autophagy activator rapamycin (MCE, MedChemExpress), were freshly dissolved in DMSO at stock concentrations of 20 mM, 100 mM, 100 mM, respectively.

Techniques: Infection, Expressing, Activation Assay, Staining