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recombinant cd137l  (MedChemExpress)


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    Structured Review

    MedChemExpress recombinant cd137l
    Expression of <t>CD137L</t> on macrophages in UUO mice. Mice were subjected to unilateral ureteral obstruction (UUO) by left ureteral ligation for 7 and 14 days. CD137L mRNA and protein expressions were detected by Real-time PCR (A) and Elisa (B). (C) Scheme of the cell-sorting approach. (D) Flow cytometric analysis and quantification of CD137L + macrophages in sham and UUO mice. kidney cell suspensions from the obstructed kidneys. (E) Immunofluorescence staining showing CD137L (green) expression and colocalization (white arrows) with F4/80 (red) in UUO kidneys. The error bars represent the SEM. ***P < 0.001. Original magnification, Scale bar, 20µm. n= 6 per group. The data were pooled from three independent experiments.
    Recombinant Cd137l, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant cd137l/product/MedChemExpress
    Average 90 stars, based on 1 article reviews
    recombinant cd137l - by Bioz Stars, 2026-03
    90/100 stars

    Images

    1) Product Images from "CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis"

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.66781

    Expression of CD137L on macrophages in UUO mice. Mice were subjected to unilateral ureteral obstruction (UUO) by left ureteral ligation for 7 and 14 days. CD137L mRNA and protein expressions were detected by Real-time PCR (A) and Elisa (B). (C) Scheme of the cell-sorting approach. (D) Flow cytometric analysis and quantification of CD137L + macrophages in sham and UUO mice. kidney cell suspensions from the obstructed kidneys. (E) Immunofluorescence staining showing CD137L (green) expression and colocalization (white arrows) with F4/80 (red) in UUO kidneys. The error bars represent the SEM. ***P < 0.001. Original magnification, Scale bar, 20µm. n= 6 per group. The data were pooled from three independent experiments.
    Figure Legend Snippet: Expression of CD137L on macrophages in UUO mice. Mice were subjected to unilateral ureteral obstruction (UUO) by left ureteral ligation for 7 and 14 days. CD137L mRNA and protein expressions were detected by Real-time PCR (A) and Elisa (B). (C) Scheme of the cell-sorting approach. (D) Flow cytometric analysis and quantification of CD137L + macrophages in sham and UUO mice. kidney cell suspensions from the obstructed kidneys. (E) Immunofluorescence staining showing CD137L (green) expression and colocalization (white arrows) with F4/80 (red) in UUO kidneys. The error bars represent the SEM. ***P < 0.001. Original magnification, Scale bar, 20µm. n= 6 per group. The data were pooled from three independent experiments.

    Techniques Used: Expressing, Ligation, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, FACS, Immunofluorescence, Staining

    VEGF-C promotes CD137L production in macrophages in vitro. (A)Relative mRNA expression of CD137L was measured in BMDMs treated with VEGF-C (0, 20, 50, 100, 1000 ng/mL) subpopulations by real-time PCR. Flow cytometric analysis and quantification showing the percentages of CD137L + MPMs (B, C) and BMDMs (D, E) with VEGF-C (100 ng/mL) and SAR131675 (23 nM). The data shown were representative FACS profiles. (F) Flow cytometric analysis showing the percentages of CD137L + BMDMs with TGF-β(10ng/mL), VEGF-C (100 ng/mL), L-1β (25ng/mL) and mixture of cytokines. The data shown were representative FACS profiles. (G) BMDMs were grown in complete medium and treated with VEGF-C (100 ng/mL) with or without SAR131675 (23 nM, 46 nM) for 48 h. Western blot analysis was performed to measure the expression of TLR4, p-P65, P65, IKK-β and GAPDH. (H) The histograms show the relative intensity for each marker normalized to GAPDH. The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001 versus control. The data were pooled from three independent experiments.
    Figure Legend Snippet: VEGF-C promotes CD137L production in macrophages in vitro. (A)Relative mRNA expression of CD137L was measured in BMDMs treated with VEGF-C (0, 20, 50, 100, 1000 ng/mL) subpopulations by real-time PCR. Flow cytometric analysis and quantification showing the percentages of CD137L + MPMs (B, C) and BMDMs (D, E) with VEGF-C (100 ng/mL) and SAR131675 (23 nM). The data shown were representative FACS profiles. (F) Flow cytometric analysis showing the percentages of CD137L + BMDMs with TGF-β(10ng/mL), VEGF-C (100 ng/mL), L-1β (25ng/mL) and mixture of cytokines. The data shown were representative FACS profiles. (G) BMDMs were grown in complete medium and treated with VEGF-C (100 ng/mL) with or without SAR131675 (23 nM, 46 nM) for 48 h. Western blot analysis was performed to measure the expression of TLR4, p-P65, P65, IKK-β and GAPDH. (H) The histograms show the relative intensity for each marker normalized to GAPDH. The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001 versus control. The data were pooled from three independent experiments.

    Techniques Used: In Vitro, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Marker, Control

    CD137L promotes the proliferation, migration and tube formation of lymphatic endothelial cells. (A) The proliferation of LECs treated with CD137L or CD137L and inhibitory for 24 h, 48 h, and 72 h was examined by CCK-8 assay. The migration of LECs was measured with the cell scratch test (B) and Transwell migration assay (D) after CD137L or CD137L and inhibitory treatment for 12 h. The histograms represent migrated (C, E) cells per field. (F) A tube formation assay was used to test the lymphangiogenesis capacity of LECs after CD137L or CD137L and inhibitory treatment for 3 h (image magnification, 100×). The histograms represent the branch number per field. (G, H, I). The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001. The data were pooled from three independent experiments.
    Figure Legend Snippet: CD137L promotes the proliferation, migration and tube formation of lymphatic endothelial cells. (A) The proliferation of LECs treated with CD137L or CD137L and inhibitory for 24 h, 48 h, and 72 h was examined by CCK-8 assay. The migration of LECs was measured with the cell scratch test (B) and Transwell migration assay (D) after CD137L or CD137L and inhibitory treatment for 12 h. The histograms represent migrated (C, E) cells per field. (F) A tube formation assay was used to test the lymphangiogenesis capacity of LECs after CD137L or CD137L and inhibitory treatment for 3 h (image magnification, 100×). The histograms represent the branch number per field. (G, H, I). The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001. The data were pooled from three independent experiments.

    Techniques Used: Migration, CCK-8 Assay, Transwell Migration Assay, Tube Formation Assay

    Transcriptome analysis of LECs after CD137L treatment (A) Eleven significantly activated KEGG pathway in SVEC4-10 cell line after treatment with CD137L. (B) Enriched KEGG pathway for differentially expressed genes in SVEC4-10 cells with or without CD137L treatment. The terms enriched from upregulated genes in CD137L treated SVEC4-10 cells are marked by red, and terms enriched from down regulated genes are marked by blue. (FDR≤0.01) (C) Top20 significantly activated biological processes in SVEC4-10 cell line after treatment with CD137L, as indicated in GO analysis (FDR≤0.01). GO, gene ontology; DEGs, differentially expressed genes; FDR, false discovery rate; KEGG, Kyoto Encyclopedia of Genes and Genomes.
    Figure Legend Snippet: Transcriptome analysis of LECs after CD137L treatment (A) Eleven significantly activated KEGG pathway in SVEC4-10 cell line after treatment with CD137L. (B) Enriched KEGG pathway for differentially expressed genes in SVEC4-10 cells with or without CD137L treatment. The terms enriched from upregulated genes in CD137L treated SVEC4-10 cells are marked by red, and terms enriched from down regulated genes are marked by blue. (FDR≤0.01) (C) Top20 significantly activated biological processes in SVEC4-10 cell line after treatment with CD137L, as indicated in GO analysis (FDR≤0.01). GO, gene ontology; DEGs, differentially expressed genes; FDR, false discovery rate; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Techniques Used:

    CD137L induced autophagy of lymphatic endothelial cells via mTOR pathway. (A) Representative electron micrographs of CD137L-induced autophagosome in SVEC4-10 cells that were either stimulated with inhibitory, or with 3-MA for 24 h. (B) The protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were analyzed in SVEC4-10 cells after CD137L, inhibitory or 3-MA treatment for 24 h by Western blot. (C) SVEC4-10 cells were infected with RFP-GFP-LC3-expressing lentivirus. Cells were untreated or treated with CD137L, inhibitory or 3-MA for 24 h. Fluorescence was examined by confocal microscopy. Transwell migration assay (D), scratch test (E) and tube formation assay (F) stimulated with CD137L for 12 h, and with or without 3-MA treatment. (G) The protein expression levels of phosphorylated PI3K, Akt and mTOR were analyzed in SVEC4-10 cells after CD137L or inhibitory or 3-MA treatment for 24 h by Western blot. (H) SVEC4-10 cells were knocked down Atg5 and Atg7 by using siRNAs, and stimulated with CD137L for 24h, the protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were detected by Western blotting.
    Figure Legend Snippet: CD137L induced autophagy of lymphatic endothelial cells via mTOR pathway. (A) Representative electron micrographs of CD137L-induced autophagosome in SVEC4-10 cells that were either stimulated with inhibitory, or with 3-MA for 24 h. (B) The protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were analyzed in SVEC4-10 cells after CD137L, inhibitory or 3-MA treatment for 24 h by Western blot. (C) SVEC4-10 cells were infected with RFP-GFP-LC3-expressing lentivirus. Cells were untreated or treated with CD137L, inhibitory or 3-MA for 24 h. Fluorescence was examined by confocal microscopy. Transwell migration assay (D), scratch test (E) and tube formation assay (F) stimulated with CD137L for 12 h, and with or without 3-MA treatment. (G) The protein expression levels of phosphorylated PI3K, Akt and mTOR were analyzed in SVEC4-10 cells after CD137L or inhibitory or 3-MA treatment for 24 h by Western blot. (H) SVEC4-10 cells were knocked down Atg5 and Atg7 by using siRNAs, and stimulated with CD137L for 24h, the protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were detected by Western blotting.

    Techniques Used: Expressing, Western Blot, Infection, Fluorescence, Confocal Microscopy, Transwell Migration Assay, Tube Formation Assay



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    Image Search Results


    Expression of CD137L on macrophages in UUO mice. Mice were subjected to unilateral ureteral obstruction (UUO) by left ureteral ligation for 7 and 14 days. CD137L mRNA and protein expressions were detected by Real-time PCR (A) and Elisa (B). (C) Scheme of the cell-sorting approach. (D) Flow cytometric analysis and quantification of CD137L + macrophages in sham and UUO mice. kidney cell suspensions from the obstructed kidneys. (E) Immunofluorescence staining showing CD137L (green) expression and colocalization (white arrows) with F4/80 (red) in UUO kidneys. The error bars represent the SEM. ***P < 0.001. Original magnification, Scale bar, 20µm. n= 6 per group. The data were pooled from three independent experiments.

    Journal: International Journal of Biological Sciences

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    doi: 10.7150/ijbs.66781

    Figure Lengend Snippet: Expression of CD137L on macrophages in UUO mice. Mice were subjected to unilateral ureteral obstruction (UUO) by left ureteral ligation for 7 and 14 days. CD137L mRNA and protein expressions were detected by Real-time PCR (A) and Elisa (B). (C) Scheme of the cell-sorting approach. (D) Flow cytometric analysis and quantification of CD137L + macrophages in sham and UUO mice. kidney cell suspensions from the obstructed kidneys. (E) Immunofluorescence staining showing CD137L (green) expression and colocalization (white arrows) with F4/80 (red) in UUO kidneys. The error bars represent the SEM. ***P < 0.001. Original magnification, Scale bar, 20µm. n= 6 per group. The data were pooled from three independent experiments.

    Article Snippet: Recombinant CD137L (Cat: HY-P7446) was purchased from MedChemExpress (Shanghai, China).

    Techniques: Expressing, Ligation, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, FACS, Immunofluorescence, Staining

    VEGF-C promotes CD137L production in macrophages in vitro. (A)Relative mRNA expression of CD137L was measured in BMDMs treated with VEGF-C (0, 20, 50, 100, 1000 ng/mL) subpopulations by real-time PCR. Flow cytometric analysis and quantification showing the percentages of CD137L + MPMs (B, C) and BMDMs (D, E) with VEGF-C (100 ng/mL) and SAR131675 (23 nM). The data shown were representative FACS profiles. (F) Flow cytometric analysis showing the percentages of CD137L + BMDMs with TGF-β(10ng/mL), VEGF-C (100 ng/mL), L-1β (25ng/mL) and mixture of cytokines. The data shown were representative FACS profiles. (G) BMDMs were grown in complete medium and treated with VEGF-C (100 ng/mL) with or without SAR131675 (23 nM, 46 nM) for 48 h. Western blot analysis was performed to measure the expression of TLR4, p-P65, P65, IKK-β and GAPDH. (H) The histograms show the relative intensity for each marker normalized to GAPDH. The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001 versus control. The data were pooled from three independent experiments.

    Journal: International Journal of Biological Sciences

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    doi: 10.7150/ijbs.66781

    Figure Lengend Snippet: VEGF-C promotes CD137L production in macrophages in vitro. (A)Relative mRNA expression of CD137L was measured in BMDMs treated with VEGF-C (0, 20, 50, 100, 1000 ng/mL) subpopulations by real-time PCR. Flow cytometric analysis and quantification showing the percentages of CD137L + MPMs (B, C) and BMDMs (D, E) with VEGF-C (100 ng/mL) and SAR131675 (23 nM). The data shown were representative FACS profiles. (F) Flow cytometric analysis showing the percentages of CD137L + BMDMs with TGF-β(10ng/mL), VEGF-C (100 ng/mL), L-1β (25ng/mL) and mixture of cytokines. The data shown were representative FACS profiles. (G) BMDMs were grown in complete medium and treated with VEGF-C (100 ng/mL) with or without SAR131675 (23 nM, 46 nM) for 48 h. Western blot analysis was performed to measure the expression of TLR4, p-P65, P65, IKK-β and GAPDH. (H) The histograms show the relative intensity for each marker normalized to GAPDH. The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001 versus control. The data were pooled from three independent experiments.

    Article Snippet: Recombinant CD137L (Cat: HY-P7446) was purchased from MedChemExpress (Shanghai, China).

    Techniques: In Vitro, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Marker, Control

    CD137L promotes the proliferation, migration and tube formation of lymphatic endothelial cells. (A) The proliferation of LECs treated with CD137L or CD137L and inhibitory for 24 h, 48 h, and 72 h was examined by CCK-8 assay. The migration of LECs was measured with the cell scratch test (B) and Transwell migration assay (D) after CD137L or CD137L and inhibitory treatment for 12 h. The histograms represent migrated (C, E) cells per field. (F) A tube formation assay was used to test the lymphangiogenesis capacity of LECs after CD137L or CD137L and inhibitory treatment for 3 h (image magnification, 100×). The histograms represent the branch number per field. (G, H, I). The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001. The data were pooled from three independent experiments.

    Journal: International Journal of Biological Sciences

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    doi: 10.7150/ijbs.66781

    Figure Lengend Snippet: CD137L promotes the proliferation, migration and tube formation of lymphatic endothelial cells. (A) The proliferation of LECs treated with CD137L or CD137L and inhibitory for 24 h, 48 h, and 72 h was examined by CCK-8 assay. The migration of LECs was measured with the cell scratch test (B) and Transwell migration assay (D) after CD137L or CD137L and inhibitory treatment for 12 h. The histograms represent migrated (C, E) cells per field. (F) A tube formation assay was used to test the lymphangiogenesis capacity of LECs after CD137L or CD137L and inhibitory treatment for 3 h (image magnification, 100×). The histograms represent the branch number per field. (G, H, I). The error bars represent the SEM. *P< 0.05, **P < 0.01; ***P < 0.001. The data were pooled from three independent experiments.

    Article Snippet: Recombinant CD137L (Cat: HY-P7446) was purchased from MedChemExpress (Shanghai, China).

    Techniques: Migration, CCK-8 Assay, Transwell Migration Assay, Tube Formation Assay

    Transcriptome analysis of LECs after CD137L treatment (A) Eleven significantly activated KEGG pathway in SVEC4-10 cell line after treatment with CD137L. (B) Enriched KEGG pathway for differentially expressed genes in SVEC4-10 cells with or without CD137L treatment. The terms enriched from upregulated genes in CD137L treated SVEC4-10 cells are marked by red, and terms enriched from down regulated genes are marked by blue. (FDR≤0.01) (C) Top20 significantly activated biological processes in SVEC4-10 cell line after treatment with CD137L, as indicated in GO analysis (FDR≤0.01). GO, gene ontology; DEGs, differentially expressed genes; FDR, false discovery rate; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Journal: International Journal of Biological Sciences

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    doi: 10.7150/ijbs.66781

    Figure Lengend Snippet: Transcriptome analysis of LECs after CD137L treatment (A) Eleven significantly activated KEGG pathway in SVEC4-10 cell line after treatment with CD137L. (B) Enriched KEGG pathway for differentially expressed genes in SVEC4-10 cells with or without CD137L treatment. The terms enriched from upregulated genes in CD137L treated SVEC4-10 cells are marked by red, and terms enriched from down regulated genes are marked by blue. (FDR≤0.01) (C) Top20 significantly activated biological processes in SVEC4-10 cell line after treatment with CD137L, as indicated in GO analysis (FDR≤0.01). GO, gene ontology; DEGs, differentially expressed genes; FDR, false discovery rate; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Article Snippet: Recombinant CD137L (Cat: HY-P7446) was purchased from MedChemExpress (Shanghai, China).

    Techniques:

    CD137L induced autophagy of lymphatic endothelial cells via mTOR pathway. (A) Representative electron micrographs of CD137L-induced autophagosome in SVEC4-10 cells that were either stimulated with inhibitory, or with 3-MA for 24 h. (B) The protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were analyzed in SVEC4-10 cells after CD137L, inhibitory or 3-MA treatment for 24 h by Western blot. (C) SVEC4-10 cells were infected with RFP-GFP-LC3-expressing lentivirus. Cells were untreated or treated with CD137L, inhibitory or 3-MA for 24 h. Fluorescence was examined by confocal microscopy. Transwell migration assay (D), scratch test (E) and tube formation assay (F) stimulated with CD137L for 12 h, and with or without 3-MA treatment. (G) The protein expression levels of phosphorylated PI3K, Akt and mTOR were analyzed in SVEC4-10 cells after CD137L or inhibitory or 3-MA treatment for 24 h by Western blot. (H) SVEC4-10 cells were knocked down Atg5 and Atg7 by using siRNAs, and stimulated with CD137L for 24h, the protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were detected by Western blotting.

    Journal: International Journal of Biological Sciences

    Article Title: CD137L-macrophage induce lymphatic endothelial cells autophagy to promote lymphangiogenesis in renal fibrosis

    doi: 10.7150/ijbs.66781

    Figure Lengend Snippet: CD137L induced autophagy of lymphatic endothelial cells via mTOR pathway. (A) Representative electron micrographs of CD137L-induced autophagosome in SVEC4-10 cells that were either stimulated with inhibitory, or with 3-MA for 24 h. (B) The protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were analyzed in SVEC4-10 cells after CD137L, inhibitory or 3-MA treatment for 24 h by Western blot. (C) SVEC4-10 cells were infected with RFP-GFP-LC3-expressing lentivirus. Cells were untreated or treated with CD137L, inhibitory or 3-MA for 24 h. Fluorescence was examined by confocal microscopy. Transwell migration assay (D), scratch test (E) and tube formation assay (F) stimulated with CD137L for 12 h, and with or without 3-MA treatment. (G) The protein expression levels of phosphorylated PI3K, Akt and mTOR were analyzed in SVEC4-10 cells after CD137L or inhibitory or 3-MA treatment for 24 h by Western blot. (H) SVEC4-10 cells were knocked down Atg5 and Atg7 by using siRNAs, and stimulated with CD137L for 24h, the protein expression levels of autophagy-associated proteins (Atg5, Atg7 and Atg12) and autophagic substrates (LC3 and p62) were detected by Western blotting.

    Article Snippet: Recombinant CD137L (Cat: HY-P7446) was purchased from MedChemExpress (Shanghai, China).

    Techniques: Expressing, Western Blot, Infection, Fluorescence, Confocal Microscopy, Transwell Migration Assay, Tube Formation Assay

    Nectin-4/CD137 Bicycle TICA cause tumor regression in vivo. (A) Jurkat-CD137 reporter cells were cocultured with CT26 clone overexpressing Nectin-4 (CT26-Nectin-4) and treated with BCY10572 (1:1 Bicycle TICA), BCY11863 (1:2 Bicycle TICA), or CD137L. Data are mean ± s.d. ( n ≥ 3 replicates). (B) Plasma concentration of BCY10572 and BCY11864 when dosed at 15 mg/kg by intraperitoneal injection to CD-1 mouse. (C, D) CT26-Nectin-4 tumor-bearing huCD137-Balb/c (C) or wild type Balb/c (D) mice were treated with daily doses of vehicle or BCY10572 (1 or 5 mg/kg) and tumor growth was monitored. Data are mean ± standard error of the mean (SEM) ( n = 5 mice/treatment cohort). TV: tumor volume.

    Journal: Journal of Medicinal Chemistry

    Article Title: Discovery and Optimization of a Synthetic Class of Nectin-4-Targeted CD137 Agonists for Immuno-oncology

    doi: 10.1021/acs.jmedchem.2c00505

    Figure Lengend Snippet: Nectin-4/CD137 Bicycle TICA cause tumor regression in vivo. (A) Jurkat-CD137 reporter cells were cocultured with CT26 clone overexpressing Nectin-4 (CT26-Nectin-4) and treated with BCY10572 (1:1 Bicycle TICA), BCY11863 (1:2 Bicycle TICA), or CD137L. Data are mean ± s.d. ( n ≥ 3 replicates). (B) Plasma concentration of BCY10572 and BCY11864 when dosed at 15 mg/kg by intraperitoneal injection to CD-1 mouse. (C, D) CT26-Nectin-4 tumor-bearing huCD137-Balb/c (C) or wild type Balb/c (D) mice were treated with daily doses of vehicle or BCY10572 (1 or 5 mg/kg) and tumor growth was monitored. Data are mean ± standard error of the mean (SEM) ( n = 5 mice/treatment cohort). TV: tumor volume.

    Article Snippet: Recombinant proteins: human CD137 (92 204B, R&D Systems) and human CD137L (2295-4L-025, R&D Systems) were purchased.

    Techniques: In Vivo, Clinical Proteomics, Concentration Assay, Injection