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pds 0330  (MedChemExpress)


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    Structured Review

    MedChemExpress pds 0330
    Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 <t>inhibitor</t> <t>PDS-0330</t> (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.
    Pds 0330, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pds 0330/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    pds 0330 - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes"

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    Journal: bioRxiv

    doi: 10.64898/2025.12.24.696454

    Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 inhibitor PDS-0330 (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.
    Figure Legend Snippet: Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 inhibitor PDS-0330 (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.

    Techniques Used: Control, Solvent, Standard Deviation

    Serum samples were collected at the time of sacrifice, and urine samples were obtained from a 24-hour urine collection performed on the day prior to sacrifice. (A) Serum glucose. (B) Serum urea nitrogen. (C) Serum creatinine. (D) Urinary albumin. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.
    Figure Legend Snippet: Serum samples were collected at the time of sacrifice, and urine samples were obtained from a 24-hour urine collection performed on the day prior to sacrifice. (A) Serum glucose. (B) Serum urea nitrogen. (C) Serum creatinine. (D) Urinary albumin. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Techniques Used: Control, Solvent

    (A) Periodic Acid–Schiff staining. Scale bars = 20 μm. (B) Transmission electron microscopy (TEM). Scale bars = 2.0 µm. (C) Podocyte foot process width measurement based on transmission electron microscopy. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.
    Figure Legend Snippet: (A) Periodic Acid–Schiff staining. Scale bars = 20 μm. (B) Transmission electron microscopy (TEM). Scale bars = 2.0 µm. (C) Podocyte foot process width measurement based on transmission electron microscopy. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Techniques Used: Staining, Transmission Assay, Electron Microscopy, Control, Solvent

    (A) Immunofluorescence analysis of claudin-1 expression on podocytes. Podocytes were identified by nephrin staining. Scale bars = 20 μm. (B) Quantification of claudin-1-positive podocyte areas, calculated as the ratio of claudin-1-positive area to the nephrin-positive podocyte area. (C) Immunofluorescence analysis of mTOR phosphorylated at serine 2448 (S2448) on podocytes. Scale bars = 20 μm. (D) Quantification of phospho-mTOR (S2448)-positive podocyte areas, calculated as the ratio of phospho-mTOR (S2448)-positive area to the nephrin-positive podocyte area. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.
    Figure Legend Snippet: (A) Immunofluorescence analysis of claudin-1 expression on podocytes. Podocytes were identified by nephrin staining. Scale bars = 20 μm. (B) Quantification of claudin-1-positive podocyte areas, calculated as the ratio of claudin-1-positive area to the nephrin-positive podocyte area. (C) Immunofluorescence analysis of mTOR phosphorylated at serine 2448 (S2448) on podocytes. Scale bars = 20 μm. (D) Quantification of phospho-mTOR (S2448)-positive podocyte areas, calculated as the ratio of phospho-mTOR (S2448)-positive area to the nephrin-positive podocyte area. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Techniques Used: Immunofluorescence, Expressing, Staining, Standard Deviation, Control, Solvent

    (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), Src, Akt phosphorylated at serine 473 (S473), Akt, mTOR phosphorylated at serine 2448 (S2448), mTOR, and Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.
    Figure Legend Snippet: (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), Src, Akt phosphorylated at serine 473 (S473), Akt, mTOR phosphorylated at serine 2448 (S2448), mTOR, and Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Techniques Used: Western Blot, Standard Deviation, Control, Solvent

    (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), total Src, Akt phosphorylated at serine 473 (S473), total Akt, mTOR phosphorylated at serine 2448 (S2448), total mTOR, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). NG, normal glucose; HG, high glucose; Ctrl, vehicle control; Inh, claudin-1 inhibitor PDS-0330.
    Figure Legend Snippet: (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), total Src, Akt phosphorylated at serine 473 (S473), total Akt, mTOR phosphorylated at serine 2448 (S2448), total mTOR, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). NG, normal glucose; HG, high glucose; Ctrl, vehicle control; Inh, claudin-1 inhibitor PDS-0330.

    Techniques Used: Western Blot, Standard Deviation, Control



    Similar Products

    pds 0330  (MedChemExpress)
    93
    MedChemExpress pds 0330
    Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 <t>inhibitor</t> <t>PDS-0330</t> (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.
    Pds 0330, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pds 0330/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    pds 0330 - by Bioz Stars, 2026-02
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 inhibitor PDS-0330 (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: Normal diet (ND)-fed or high-fat diet (HFD)-fed mice were orally administered either the claudin-1 inhibitor PDS-0330 (Inh) or a control solvent (Ctrl) once weekly from 15 weeks of age for 4 weeks. (A) Timeline of mouse feeding and drug administration. (B) Body weight changes during diet feeding and Inh administration. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05 for ND-Ctrl vs. HFD-Ctrl.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Control, Solvent, Standard Deviation

    Serum samples were collected at the time of sacrifice, and urine samples were obtained from a 24-hour urine collection performed on the day prior to sacrifice. (A) Serum glucose. (B) Serum urea nitrogen. (C) Serum creatinine. (D) Urinary albumin. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: Serum samples were collected at the time of sacrifice, and urine samples were obtained from a 24-hour urine collection performed on the day prior to sacrifice. (A) Serum glucose. (B) Serum urea nitrogen. (C) Serum creatinine. (D) Urinary albumin. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Control, Solvent

    (A) Periodic Acid–Schiff staining. Scale bars = 20 μm. (B) Transmission electron microscopy (TEM). Scale bars = 2.0 µm. (C) Podocyte foot process width measurement based on transmission electron microscopy. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: (A) Periodic Acid–Schiff staining. Scale bars = 20 μm. (B) Transmission electron microscopy (TEM). Scale bars = 2.0 µm. (C) Podocyte foot process width measurement based on transmission electron microscopy. Differences were evaluated by two-way ANOVA followed by the Tukey–Kramer test; * p < 0.05. ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Staining, Transmission Assay, Electron Microscopy, Control, Solvent

    (A) Immunofluorescence analysis of claudin-1 expression on podocytes. Podocytes were identified by nephrin staining. Scale bars = 20 μm. (B) Quantification of claudin-1-positive podocyte areas, calculated as the ratio of claudin-1-positive area to the nephrin-positive podocyte area. (C) Immunofluorescence analysis of mTOR phosphorylated at serine 2448 (S2448) on podocytes. Scale bars = 20 μm. (D) Quantification of phospho-mTOR (S2448)-positive podocyte areas, calculated as the ratio of phospho-mTOR (S2448)-positive area to the nephrin-positive podocyte area. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: (A) Immunofluorescence analysis of claudin-1 expression on podocytes. Podocytes were identified by nephrin staining. Scale bars = 20 μm. (B) Quantification of claudin-1-positive podocyte areas, calculated as the ratio of claudin-1-positive area to the nephrin-positive podocyte area. (C) Immunofluorescence analysis of mTOR phosphorylated at serine 2448 (S2448) on podocytes. Scale bars = 20 μm. (D) Quantification of phospho-mTOR (S2448)-positive podocyte areas, calculated as the ratio of phospho-mTOR (S2448)-positive area to the nephrin-positive podocyte area. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Immunofluorescence, Expressing, Staining, Standard Deviation, Control, Solvent

    (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), Src, Akt phosphorylated at serine 473 (S473), Akt, mTOR phosphorylated at serine 2448 (S2448), mTOR, and Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), Src, Akt phosphorylated at serine 473 (S473), Akt, mTOR phosphorylated at serine 2448 (S2448), mTOR, and Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). ND, normal diet; HFD, high-fat diet; Ctrl, control solvent; Inh, claudin-1 inhibitor PDS-0330.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Western Blot, Standard Deviation, Control, Solvent

    (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), total Src, Akt phosphorylated at serine 473 (S473), total Akt, mTOR phosphorylated at serine 2448 (S2448), total mTOR, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). NG, normal glucose; HG, high glucose; Ctrl, vehicle control; Inh, claudin-1 inhibitor PDS-0330.

    Journal: bioRxiv

    Article Title: Claudin-1 Inhibitor PDS-0330 Ameliorates Diabetic Kidney Disease by Suppressing Src/Akt/mTOR Signaling Pathway in Podocytes

    doi: 10.64898/2025.12.24.696454

    Figure Lengend Snippet: (A) Western blotting analysis of claudin-1, Src phosphorylated at tyrosine 416 (Y416), total Src, Akt phosphorylated at serine 473 (S473), total Akt, mTOR phosphorylated at serine 2448 (S2448), total mTOR, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). (B-E) Densitometric analysis was performed to quantify the western blotting results. Results are presented as the mean ± standard deviation. Differences were evaluated by two-way ANOVA followed by Tukey–Kramer test (* p < 0.05). NG, normal glucose; HG, high glucose; Ctrl, vehicle control; Inh, claudin-1 inhibitor PDS-0330.

    Article Snippet: After ten weeks of feeding, we orally administrated 5 mg/kg PDS-0330 (MedChemExpress LLC, Monmouth Junction, NJ, USA) dissolved in a solvent consisting of 5% dimethyl sulfoxide (DMSO), 40% polyethylene glycol 300 (PEG300), 5% polyoxyethylene (20) sorbitan monooleate (Tween-80) and 50% double-distilled water or the solvent (as control) once weekly for 4 weeks.

    Techniques: Western Blot, Standard Deviation, Control