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MedChemExpress stat 3 inhibitor s3i 201

Majoon Ushba ablates the <t>IL-17A-JAK-2/STAT-3</t> signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Stat 3 Inhibitor S3i 201, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stat+3+inhibitor+s3i+201/pmc13078650-138-1-12?v=MedChemExpress
Average 96 stars, based on 88 article reviews

stat 3 inhibitor s3i 201 - by Bioz Stars, 2026-07

96/100 stars

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1) Product Images from "Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation"

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

Journal: Pharmaceutical Biology

doi: 10.1080/13880209.2026.2654904

Majoon Ushba ablates the IL-17A-JAK-2/STAT-3 signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Figure Legend Snippet: Majoon Ushba ablates the IL-17A-JAK-2/STAT-3 signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Techniques Used: Expressing, Immunofluorescence, Translocation Assay, Colony Assay

Pharmacological ablation of psoriasis pathogenic mediators by Majoon Ushba via attenuating JAK-2-STAT-3 signaling axis. (A–C) Relative gene expression of Cyr61, HMGB1, and VEGF was assessed using RT-PCR. (D–F) Relative protein expression was assessed using immunofluorescence, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes.

Figure Legend Snippet: Pharmacological ablation of psoriasis pathogenic mediators by Majoon Ushba via attenuating JAK-2-STAT-3 signaling axis. (A–C) Relative gene expression of Cyr61, HMGB1, and VEGF was assessed using RT-PCR. (D–F) Relative protein expression was assessed using immunofluorescence, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes.

Techniques Used: Gene Expression, Reverse Transcription Polymerase Chain Reaction, Expressing, Immunofluorescence

Majoon Ushba abrogated the JAK-2-STAT-3 signaling axis in an IMQ-induced psoriasis mice model. Skin tissue from mice in the respective experimental groups was obtained following euthanasia and used to isolate total protein and RNA. (A) Relative protein levels of JAK-2, p-JAK2, STAT-3, and p-STAT3 were assessed using western blotting. (B) Additionally, the protein levels of Ki67, a cell proliferation marker, and p-STAT3 were assessed using immunohistochemistry, magnification: 20X, Scale bar: 100μm. Total RNA was used to measure the relative mRNA levels of (C) Cyr61, (D) HMGB1, and (E) VEGF by RT-PCR. The values are expressed as the mean ± SEM of n = 6 animal per group. Each data point (n = 6 per group) represents the average of three technical replicates. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: #p < 0.05, ##p < 0.01 and ### p < 0.01 verses control mice. * p < 0.05, ** p < 0.01 and *** p < 0.01 verses IMQ-induced psoriasis mice. Abbreviations: Cyr61, cysteine-rich angiogenic inducer 61; HMGB, High mobility group box 1; VEGF, Vascular endothelial growth factor.

Figure Legend Snippet: Majoon Ushba abrogated the JAK-2-STAT-3 signaling axis in an IMQ-induced psoriasis mice model. Skin tissue from mice in the respective experimental groups was obtained following euthanasia and used to isolate total protein and RNA. (A) Relative protein levels of JAK-2, p-JAK2, STAT-3, and p-STAT3 were assessed using western blotting. (B) Additionally, the protein levels of Ki67, a cell proliferation marker, and p-STAT3 were assessed using immunohistochemistry, magnification: 20X, Scale bar: 100μm. Total RNA was used to measure the relative mRNA levels of (C) Cyr61, (D) HMGB1, and (E) VEGF by RT-PCR. The values are expressed as the mean ± SEM of n = 6 animal per group. Each data point (n = 6 per group) represents the average of three technical replicates. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: #p < 0.05, ##p < 0.01 and ### p < 0.01 verses control mice. * p < 0.05, ** p < 0.01 and *** p < 0.01 verses IMQ-induced psoriasis mice. Abbreviations: Cyr61, cysteine-rich angiogenic inducer 61; HMGB, High mobility group box 1; VEGF, Vascular endothelial growth factor.

Techniques Used: Western Blot, Marker, Immunohistochemistry, Reverse Transcription Polymerase Chain Reaction, Control

In-Silico molecular docking analysis revealed strong binding partners against IL-17RA and STAT-3. (A–C) The prospective phytoconstituents catechin, morin, and quercetin, docked against IL-17R, showed stable interactions. (D–F) The phytoconstituents, Catechin, Morin and Quercetin docked against STAT-3 showing stable interactions.

Figure Legend Snippet: In-Silico molecular docking analysis revealed strong binding partners against IL-17RA and STAT-3. (A–C) The prospective phytoconstituents catechin, morin, and quercetin, docked against IL-17R, showed stable interactions. (D–F) The phytoconstituents, Catechin, Morin and Quercetin docked against STAT-3 showing stable interactions.

Techniques Used: In Silico, Binding Assay

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Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Majoon Ushba ablates the IL-17A-JAK-2/STAT-3 signaling axis. (A) Relative protein expression of JAK-2, p-JAK-2, STAT-3, and p-STAT3 in IL-17A stimulated HaCaT cells. (B) Immunofluorescence of p-STAT3 to assess nuclear translocation. (C) Colony formation assay was performed to assess the ability of the IL-17A/JAK-2-STAT-3 pathway to influence cell proliferation, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes. Abbreviations: JAK-2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; IL-17A, Interleukin 17 A.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Expressing, Immunofluorescence, Translocation Assay, Colony Assay

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Pharmacological ablation of psoriasis pathogenic mediators by Majoon Ushba via attenuating JAK-2-STAT-3 signaling axis. (A–C) Relative gene expression of Cyr61, HMGB1, and VEGF was assessed using RT-PCR. (D–F) Relative protein expression was assessed using immunofluorescence, magnification: 20X, Scale bar: 100μm. Data are expressed as the mean ± SEM of n = 3 independent biological replicates (separate experiments). Each dot represents a single biological replicate from one independent experiment. Mean difference and confidence intervals are shown in the supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: # ( p < 0.05), ## ( p < 0.01), and ### ( p < 0.001) versus untreated HaCaT keratinocytes; * ( p < 0.05), ** p < 0.01, and *** p < 0.001 versus IL-17A-stimulated psoriasis-like keratinocytes.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Gene Expression, Reverse Transcription Polymerase Chain Reaction, Expressing, Immunofluorescence

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: Majoon Ushba abrogated the JAK-2-STAT-3 signaling axis in an IMQ-induced psoriasis mice model. Skin tissue from mice in the respective experimental groups was obtained following euthanasia and used to isolate total protein and RNA. (A) Relative protein levels of JAK-2, p-JAK2, STAT-3, and p-STAT3 were assessed using western blotting. (B) Additionally, the protein levels of Ki67, a cell proliferation marker, and p-STAT3 were assessed using immunohistochemistry, magnification: 20X, Scale bar: 100μm. Total RNA was used to measure the relative mRNA levels of (C) Cyr61, (D) HMGB1, and (E) VEGF by RT-PCR. The values are expressed as the mean ± SEM of n = 6 animal per group. Each data point (n = 6 per group) represents the average of three technical replicates. Mean difference and confidence intervals are shown in the Supplementary Table 1 . Statistical significance was determined by one-way ANOVA followed by Bonferroni’s post-hoc test: #p < 0.05, ##p < 0.01 and ### p < 0.01 verses control mice. * p < 0.05, ** p < 0.01 and *** p < 0.01 verses IMQ-induced psoriasis mice. Abbreviations: Cyr61, cysteine-rich angiogenic inducer 61; HMGB, High mobility group box 1; VEGF, Vascular endothelial growth factor.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: Western Blot, Marker, Immunohistochemistry, Reverse Transcription Polymerase Chain Reaction, Control

Journal: Pharmaceutical Biology

Article Title: Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation

doi: 10.1080/13880209.2026.2654904

Figure Lengend Snippet: In-Silico molecular docking analysis revealed strong binding partners against IL-17RA and STAT-3. (A–C) The prospective phytoconstituents catechin, morin, and quercetin, docked against IL-17R, showed stable interactions. (D–F) The phytoconstituents, Catechin, Morin and Quercetin docked against STAT-3 showing stable interactions.

Article Snippet: The STAT-3 inhibitor S3I-201 and canonical ferroptosis inhibitor (ferrostain-1) were purchased from MedChem Express (NJ, USA).

Techniques: In Silico, Binding Assay

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