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ca9 inhibitor s4  (MedChemExpress)


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    MedChemExpress ca9 inhibitor s4
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Ca9 Inhibitor S4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/caix/CAIX+Inhibitor+S4/pmc13084789-105-0-3
    Average 94 stars, based on 2 article reviews
    ca9 inhibitor s4 - by Bioz Stars, 2026-10
    94/100 stars

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    1) Product Images from "Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab"

    Article Title: Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1136/jitc-2025-013384

    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Figure Legend Snippet: High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.

    Techniques Used: High Throughput Screening Assay, Clinical Proteomics, Comparison, Control, Modification

    Patients with unresectable HCC with high plasma CA9 levels are associated with poor disease control and shorter survival on Atez/Bev therapy. 89 patients with unresectable HCC treated with Atez/Bev therapy were enrolled in the validation cohort. ( A–B ) Plasma CA9 levels in patients with HCC who achieved disease control with Atez/Bev treatment and those with progressive disease, evaluated by RECIST (A) and mRECIST (B). Each dot represents one patient. ( C ) ROC curve of plasma CA9 levels for predicting initial PD; the area under the ROC curve is shown. ( D ) Proportions of patients with DC or PD stratified by high versus low plasma CA9 levels, according to RECIST (left) and mRECIST (right), based on the CA9 cut-off defined in ( C ). ( E, F ) Kaplan-Meier curves for PFS stratified by high versus low plasma CA9 levels, assessed by ( E ) RECIST and ( F ) mRECIST. ( G ) Kaplan-Meier curves for OS stratified by plasma CA9 level in the same cohort. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test, or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CR, complete response; DC, disease control; DCR, disease control rate; HCC, hepatocellular carcinoma; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; OS, overall survival; PD, progressive disease; PR, partial response; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; ROC, receiver operating characteristic; SD, stable disease.
    Figure Legend Snippet: Patients with unresectable HCC with high plasma CA9 levels are associated with poor disease control and shorter survival on Atez/Bev therapy. 89 patients with unresectable HCC treated with Atez/Bev therapy were enrolled in the validation cohort. ( A–B ) Plasma CA9 levels in patients with HCC who achieved disease control with Atez/Bev treatment and those with progressive disease, evaluated by RECIST (A) and mRECIST (B). Each dot represents one patient. ( C ) ROC curve of plasma CA9 levels for predicting initial PD; the area under the ROC curve is shown. ( D ) Proportions of patients with DC or PD stratified by high versus low plasma CA9 levels, according to RECIST (left) and mRECIST (right), based on the CA9 cut-off defined in ( C ). ( E, F ) Kaplan-Meier curves for PFS stratified by high versus low plasma CA9 levels, assessed by ( E ) RECIST and ( F ) mRECIST. ( G ) Kaplan-Meier curves for OS stratified by plasma CA9 level in the same cohort. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test, or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CR, complete response; DC, disease control; DCR, disease control rate; HCC, hepatocellular carcinoma; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; OS, overall survival; PD, progressive disease; PR, partial response; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; ROC, receiver operating characteristic; SD, stable disease.

    Techniques Used: Clinical Proteomics, Control, Biomarker Discovery, Modification

    Tumorous CA9 may be the source of circulating CA9 and confers resistance to the combination immunotherapy of anti-PD-L1 and anti-VEGF antibodies in HCC. ( A–C ) Single-cell RNA sequencing data from the HCCDB V.2.0 (Lifeome) portal showing ( A ) UMAP of major cell types and feature plots of ( B ) CA9 and ( C ) AFP expression. ( D ) Western blot analysis of Car9 and Actb in Hep55.1c cells with NC or Car9 OE. ( E ) mRNA levels of Car9 in syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control or Car9 overexpression (NC: n=28; OE: n=25). ( F ) Growth curves of syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control (left) or Car9 overexpression (right) (n=8 per group). ( G ) Tumor volume 14 days after inoculation in NC and OE tumors (NC: n=28; OE: n=25). ( H ) Growth curves of syngeneic subcutaneous tumors derived from NC or Car9-overexpression Hep55.1c cells treated with vehicle or anti-PD-L1/VEGF antibodies (treatment) (n=8 per group). ( I ) Relative treatment response calculated for each mouse as the tumor volume in the anti-PD-L1/VEGF-treated group divided by the mean tumor volume of the corresponding vehicle-treated group within the same genotype (NC or Car9 OE) at day 14. Each dot represents an individual tumor, allowing comparison of relative treatment effects between NC-derived and Car9-OE-derived tumors. Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or two-way repeated-measures ANOVA, as appropriate; p<0.05 was considered statistically significant. AFP, alpha-fetoprotein; ANOVA, analysis of variance; CA9, carbonic anhydrase 9; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor.
    Figure Legend Snippet: Tumorous CA9 may be the source of circulating CA9 and confers resistance to the combination immunotherapy of anti-PD-L1 and anti-VEGF antibodies in HCC. ( A–C ) Single-cell RNA sequencing data from the HCCDB V.2.0 (Lifeome) portal showing ( A ) UMAP of major cell types and feature plots of ( B ) CA9 and ( C ) AFP expression. ( D ) Western blot analysis of Car9 and Actb in Hep55.1c cells with NC or Car9 OE. ( E ) mRNA levels of Car9 in syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control or Car9 overexpression (NC: n=28; OE: n=25). ( F ) Growth curves of syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control (left) or Car9 overexpression (right) (n=8 per group). ( G ) Tumor volume 14 days after inoculation in NC and OE tumors (NC: n=28; OE: n=25). ( H ) Growth curves of syngeneic subcutaneous tumors derived from NC or Car9-overexpression Hep55.1c cells treated with vehicle or anti-PD-L1/VEGF antibodies (treatment) (n=8 per group). ( I ) Relative treatment response calculated for each mouse as the tumor volume in the anti-PD-L1/VEGF-treated group divided by the mean tumor volume of the corresponding vehicle-treated group within the same genotype (NC or Car9 OE) at day 14. Each dot represents an individual tumor, allowing comparison of relative treatment effects between NC-derived and Car9-OE-derived tumors. Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or two-way repeated-measures ANOVA, as appropriate; p<0.05 was considered statistically significant. AFP, alpha-fetoprotein; ANOVA, analysis of variance; CA9, carbonic anhydrase 9; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor.

    Techniques Used: Single Cell, RNA Sequencing, Expressing, Western Blot, Derivative Assay, Negative Control, Over Expression, Comparison, Two Tailed Test

    Tumorous CA9 flourishes the immunosuppressive and angiogenic tumor microenvironment in HCC. ( A–C ) Relative mRNA expression of the indicated genes in syngeneic subcutaneous tumors derived from Hep55.1c cells with NC or Car9 OE, measured by quantitative RT-PCR (NC: n=28; OE: n=25). Each dot represents one tumor; bars indicate mean±SEM. ( D ) UMAP of single-cell RNA sequencing data from NC and CA9 OE tumors, colored by annotated cell type (eg, malignant cells, T cells, TAMs, endothelial cells). ( E ) Frequency of CTLs per tumor sample, calculated as CTLs divided by total cells profiled by scRNA-seq (NC: n=3; CA9 OE: n=3). ( F, G ) Differential gene expression and representative cytotoxicity-related genes in CD8 + T cells from CA9 OE versus NC tumors. ( H, I ) Differential gene expression and representative TAM-related genes in TAMs from CA9 OE versus NC tumors. ( J–L ) Gene Set Enrichment Analysis (Gene Ontology) showed the top 20 pathways in TAMs ( J ), dendritic cells ( K ), and endothelial cells ( L ). ( M ) Tumor growth curves of syngeneic subcutaneous tumors derived from Car9-overexpressing Hep55.1c cells treated with vehicle, CA9 inhibitor alone, anti-PD-L1 plus anti-VEGF antibodies (Combi), or Combi plus CA9 inhibitor (Combi+CA9 inhibitor) (n=8–12 per group). Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or Wilcoxon rank-sum tests, as appropriate; p<0.05 was considered statistically significant. CAF, cancer-associated fibroblast; CA9, carbonic anhydrase 9; CTLs, cytotoxic T lymphocytes; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; RT-PCR, reverse transcription PCR; scRNA-seq, single-cell RNA sequencing; TAM, tumor-associated macrophage; TAN, tumor-associated neutrophils; TPM, transcripts per million; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor; WT, wild type.
    Figure Legend Snippet: Tumorous CA9 flourishes the immunosuppressive and angiogenic tumor microenvironment in HCC. ( A–C ) Relative mRNA expression of the indicated genes in syngeneic subcutaneous tumors derived from Hep55.1c cells with NC or Car9 OE, measured by quantitative RT-PCR (NC: n=28; OE: n=25). Each dot represents one tumor; bars indicate mean±SEM. ( D ) UMAP of single-cell RNA sequencing data from NC and CA9 OE tumors, colored by annotated cell type (eg, malignant cells, T cells, TAMs, endothelial cells). ( E ) Frequency of CTLs per tumor sample, calculated as CTLs divided by total cells profiled by scRNA-seq (NC: n=3; CA9 OE: n=3). ( F, G ) Differential gene expression and representative cytotoxicity-related genes in CD8 + T cells from CA9 OE versus NC tumors. ( H, I ) Differential gene expression and representative TAM-related genes in TAMs from CA9 OE versus NC tumors. ( J–L ) Gene Set Enrichment Analysis (Gene Ontology) showed the top 20 pathways in TAMs ( J ), dendritic cells ( K ), and endothelial cells ( L ). ( M ) Tumor growth curves of syngeneic subcutaneous tumors derived from Car9-overexpressing Hep55.1c cells treated with vehicle, CA9 inhibitor alone, anti-PD-L1 plus anti-VEGF antibodies (Combi), or Combi plus CA9 inhibitor (Combi+CA9 inhibitor) (n=8–12 per group). Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or Wilcoxon rank-sum tests, as appropriate; p<0.05 was considered statistically significant. CAF, cancer-associated fibroblast; CA9, carbonic anhydrase 9; CTLs, cytotoxic T lymphocytes; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; RT-PCR, reverse transcription PCR; scRNA-seq, single-cell RNA sequencing; TAM, tumor-associated macrophage; TAN, tumor-associated neutrophils; TPM, transcripts per million; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor; WT, wild type.

    Techniques Used: Expressing, Derivative Assay, Quantitative RT-PCR, Single Cell, RNA Sequencing, Gene Expression, Two Tailed Test, Negative Control, Over Expression, Reverse Transcription Polymerase Chain Reaction, Reverse Transcription

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    Article Snippet: The CAIX inhibitor U-104 was purchased from MedChemExpress (product no. HY-13513, Monmouth Junction, New Jersey, USA).

    Recombinant:

    Article Title: HVEM costimulatory domain boosts CAR T cell efficacy against solid tumors via enhanced TRAF-mediated TNF signaling.
    Article Snippet: Penicillin/streptomycin solution and fetal bovine serum (FBS) were bought from BioChannel Biotechnology Co., Ltd (Nanjing, China). .. In addition, DynabeadsTM Human T-Activator CD3/CD28 was obtained from Gibco (11132D), recombinant human IL-2 (rhIL-2) was purchased from PrimeGene (Shanghai, China), and recombinant human carbonic anhydrase 9 (rhCAIX) was obtained from MedChemExpress (Shanghai, China). ..

    Article Title: HVEM costimulatory domain boosts CAR T cell efficacy against solid tumors via enhanced TRAF-mediated TNF signaling
    Article Snippet: Penicillin/streptomycin solution and fetal bovine serum (FBS) were bought from BioChannel Biotechnology Co., Ltd (Nanjing, China). .. In addition, DynabeadsTM Human T-Activator CD3/CD28 was obtained from Gibco (11132D), recombinant human IL-2 (rhIL-2) was purchased from PrimeGene (Shanghai, China), and recombinant human carbonic anhydrase 9 (rhCAIX) was obtained from MedChemExpress (Shanghai, China). ..

    Synthesized:

    Article Title: Electron Paramagnetic Resonance Implemented with Multiple Harmonic Detections Successfully Maps Extracellular pH In Vivo.
    Article Snippet: Extracellular acidification indicates a metabolic shift in cancer cells and is, along with tissue hypoxia, a hallmark of tumor malignancy.. Thus, non-invasive mapping of extracellular pH (pHe) is essential for researchers to understand the tumor microenvironment and to monitor tumor response to metabolismtargeting drugs.. While electron paramagnetic resonance (EPR) has been successfully used to map pHe in mouse xenograft models, this method is not sensitive enough to map pHe with a moderate amount of exogenous pH-sensitive probes.



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    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Carbonic Anhydrase Ix Caix, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    antibodies against caix a1658  (ABclonal Biotechnology)
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    ABclonal Biotechnology antibodies against caix a1658
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Antibodies Against Caix A1658, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human caix protein  (Sino Biological)
    94
    Sino Biological human caix protein
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Human Caix Protein, supplied by Sino Biological, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit polyclonal anti caix antibody  (Proteintech)
    95
    Proteintech rabbit polyclonal anti caix antibody
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Rabbit Polyclonal Anti Caix Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti caix antibody  (Novus Biologicals)
    94
    Novus Biologicals anti caix antibody
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Anti Caix Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    caix  (Human Protein Atlas)
    86
    Human Protein Atlas caix
    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma <t>CA9</t> levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.
    Caix, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab

    doi: 10.1136/jitc-2025-013384

    Figure Lengend Snippet: High-throughput proteomics identifies circulating proteins correlated with the response to Atez and Bev treatment in unresectable HCC. 78 patients with unresectable HCC treated with Atez/Bev were included in the discovery cohort. ( A–B ) Volcano plots showing plasma levels of 92 immune-oncology-related proteins measured by Olink in patients who achieved DC versus those with PD, evaluated by ( A ) RECIST and ( B ) mRECIST. The x-axis indicates log₂ fold-change of protein levels in PD versus DC, and the y-axis indicates –log₁₀ (p) values for the comparison between the two groups. ( C ) ORR and DCR of patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by mRECIST. ( D–E ) Kaplan-Meier PFS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy evaluated by RECIST ( D ) and mRECIST ( E ). ( F ) Kaplan-Meier OS curves for patients with high and low plasma CA9 levels on Atez/Bev therapy. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CSF, colony-stimulating factor; DC, disease control; DCR, disease control rate; FC, fold change; HCC, hepatocellular carcinoma; IL, interleukin; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; MCP-3, monocyte chemoattractant protein 3; MMP12, matrix metalloproteinase 12; mORR, objective response rate by mRECIST; OS, overall survival; ORR, overall response rate; PD, progressive disease; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; VEGF, vascular endothelial growth factor.

    Article Snippet: CA9 inhibitor S4 (MedChemExpress, Cat# HY-110243; 5 mg/kg, i.p.).

    Techniques: High Throughput Screening Assay, Clinical Proteomics, Comparison, Control, Modification

    Patients with unresectable HCC with high plasma CA9 levels are associated with poor disease control and shorter survival on Atez/Bev therapy. 89 patients with unresectable HCC treated with Atez/Bev therapy were enrolled in the validation cohort. ( A–B ) Plasma CA9 levels in patients with HCC who achieved disease control with Atez/Bev treatment and those with progressive disease, evaluated by RECIST (A) and mRECIST (B). Each dot represents one patient. ( C ) ROC curve of plasma CA9 levels for predicting initial PD; the area under the ROC curve is shown. ( D ) Proportions of patients with DC or PD stratified by high versus low plasma CA9 levels, according to RECIST (left) and mRECIST (right), based on the CA9 cut-off defined in ( C ). ( E, F ) Kaplan-Meier curves for PFS stratified by high versus low plasma CA9 levels, assessed by ( E ) RECIST and ( F ) mRECIST. ( G ) Kaplan-Meier curves for OS stratified by plasma CA9 level in the same cohort. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test, or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CR, complete response; DC, disease control; DCR, disease control rate; HCC, hepatocellular carcinoma; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; OS, overall survival; PD, progressive disease; PR, partial response; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; ROC, receiver operating characteristic; SD, stable disease.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab

    doi: 10.1136/jitc-2025-013384

    Figure Lengend Snippet: Patients with unresectable HCC with high plasma CA9 levels are associated with poor disease control and shorter survival on Atez/Bev therapy. 89 patients with unresectable HCC treated with Atez/Bev therapy were enrolled in the validation cohort. ( A–B ) Plasma CA9 levels in patients with HCC who achieved disease control with Atez/Bev treatment and those with progressive disease, evaluated by RECIST (A) and mRECIST (B). Each dot represents one patient. ( C ) ROC curve of plasma CA9 levels for predicting initial PD; the area under the ROC curve is shown. ( D ) Proportions of patients with DC or PD stratified by high versus low plasma CA9 levels, according to RECIST (left) and mRECIST (right), based on the CA9 cut-off defined in ( C ). ( E, F ) Kaplan-Meier curves for PFS stratified by high versus low plasma CA9 levels, assessed by ( E ) RECIST and ( F ) mRECIST. ( G ) Kaplan-Meier curves for OS stratified by plasma CA9 level in the same cohort. Group comparisons were performed using appropriate statistical tests (eg, χ 2 test, or log-rank test), as detailed in the Methods; p<0.05 was considered statistically significant. Atez, atezolizumab; Bev, bevacizumab; CA9, carbonic anhydrase 9; CR, complete response; DC, disease control; DCR, disease control rate; HCC, hepatocellular carcinoma; mDCR, disease control rate by mRECIST; mPFS, modified PFS; mRECIST, modified RECIST; OS, overall survival; PD, progressive disease; PR, partial response; PFS, progression-free survival; RECIST, Response Evaluation Criteria in Solid Tumors; ROC, receiver operating characteristic; SD, stable disease.

    Article Snippet: CA9 inhibitor S4 (MedChemExpress, Cat# HY-110243; 5 mg/kg, i.p.).

    Techniques: Clinical Proteomics, Control, Biomarker Discovery, Modification

    Tumorous CA9 may be the source of circulating CA9 and confers resistance to the combination immunotherapy of anti-PD-L1 and anti-VEGF antibodies in HCC. ( A–C ) Single-cell RNA sequencing data from the HCCDB V.2.0 (Lifeome) portal showing ( A ) UMAP of major cell types and feature plots of ( B ) CA9 and ( C ) AFP expression. ( D ) Western blot analysis of Car9 and Actb in Hep55.1c cells with NC or Car9 OE. ( E ) mRNA levels of Car9 in syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control or Car9 overexpression (NC: n=28; OE: n=25). ( F ) Growth curves of syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control (left) or Car9 overexpression (right) (n=8 per group). ( G ) Tumor volume 14 days after inoculation in NC and OE tumors (NC: n=28; OE: n=25). ( H ) Growth curves of syngeneic subcutaneous tumors derived from NC or Car9-overexpression Hep55.1c cells treated with vehicle or anti-PD-L1/VEGF antibodies (treatment) (n=8 per group). ( I ) Relative treatment response calculated for each mouse as the tumor volume in the anti-PD-L1/VEGF-treated group divided by the mean tumor volume of the corresponding vehicle-treated group within the same genotype (NC or Car9 OE) at day 14. Each dot represents an individual tumor, allowing comparison of relative treatment effects between NC-derived and Car9-OE-derived tumors. Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or two-way repeated-measures ANOVA, as appropriate; p<0.05 was considered statistically significant. AFP, alpha-fetoprotein; ANOVA, analysis of variance; CA9, carbonic anhydrase 9; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab

    doi: 10.1136/jitc-2025-013384

    Figure Lengend Snippet: Tumorous CA9 may be the source of circulating CA9 and confers resistance to the combination immunotherapy of anti-PD-L1 and anti-VEGF antibodies in HCC. ( A–C ) Single-cell RNA sequencing data from the HCCDB V.2.0 (Lifeome) portal showing ( A ) UMAP of major cell types and feature plots of ( B ) CA9 and ( C ) AFP expression. ( D ) Western blot analysis of Car9 and Actb in Hep55.1c cells with NC or Car9 OE. ( E ) mRNA levels of Car9 in syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control or Car9 overexpression (NC: n=28; OE: n=25). ( F ) Growth curves of syngeneic subcutaneous tumors derived from Hep55.1c cells with either negative control (left) or Car9 overexpression (right) (n=8 per group). ( G ) Tumor volume 14 days after inoculation in NC and OE tumors (NC: n=28; OE: n=25). ( H ) Growth curves of syngeneic subcutaneous tumors derived from NC or Car9-overexpression Hep55.1c cells treated with vehicle or anti-PD-L1/VEGF antibodies (treatment) (n=8 per group). ( I ) Relative treatment response calculated for each mouse as the tumor volume in the anti-PD-L1/VEGF-treated group divided by the mean tumor volume of the corresponding vehicle-treated group within the same genotype (NC or Car9 OE) at day 14. Each dot represents an individual tumor, allowing comparison of relative treatment effects between NC-derived and Car9-OE-derived tumors. Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or two-way repeated-measures ANOVA, as appropriate; p<0.05 was considered statistically significant. AFP, alpha-fetoprotein; ANOVA, analysis of variance; CA9, carbonic anhydrase 9; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor.

    Article Snippet: CA9 inhibitor S4 (MedChemExpress, Cat# HY-110243; 5 mg/kg, i.p.).

    Techniques: Single Cell, RNA Sequencing, Expressing, Western Blot, Derivative Assay, Negative Control, Over Expression, Comparison, Two Tailed Test

    Tumorous CA9 flourishes the immunosuppressive and angiogenic tumor microenvironment in HCC. ( A–C ) Relative mRNA expression of the indicated genes in syngeneic subcutaneous tumors derived from Hep55.1c cells with NC or Car9 OE, measured by quantitative RT-PCR (NC: n=28; OE: n=25). Each dot represents one tumor; bars indicate mean±SEM. ( D ) UMAP of single-cell RNA sequencing data from NC and CA9 OE tumors, colored by annotated cell type (eg, malignant cells, T cells, TAMs, endothelial cells). ( E ) Frequency of CTLs per tumor sample, calculated as CTLs divided by total cells profiled by scRNA-seq (NC: n=3; CA9 OE: n=3). ( F, G ) Differential gene expression and representative cytotoxicity-related genes in CD8 + T cells from CA9 OE versus NC tumors. ( H, I ) Differential gene expression and representative TAM-related genes in TAMs from CA9 OE versus NC tumors. ( J–L ) Gene Set Enrichment Analysis (Gene Ontology) showed the top 20 pathways in TAMs ( J ), dendritic cells ( K ), and endothelial cells ( L ). ( M ) Tumor growth curves of syngeneic subcutaneous tumors derived from Car9-overexpressing Hep55.1c cells treated with vehicle, CA9 inhibitor alone, anti-PD-L1 plus anti-VEGF antibodies (Combi), or Combi plus CA9 inhibitor (Combi+CA9 inhibitor) (n=8–12 per group). Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or Wilcoxon rank-sum tests, as appropriate; p<0.05 was considered statistically significant. CAF, cancer-associated fibroblast; CA9, carbonic anhydrase 9; CTLs, cytotoxic T lymphocytes; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; RT-PCR, reverse transcription PCR; scRNA-seq, single-cell RNA sequencing; TAM, tumor-associated macrophage; TAN, tumor-associated neutrophils; TPM, transcripts per million; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor; WT, wild type.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Carbonic anhydrase 9 as a circulating biomarker and therapeutic target in patients with hepatocellular carcinoma treated with atezolizumab plus bevacizumab

    doi: 10.1136/jitc-2025-013384

    Figure Lengend Snippet: Tumorous CA9 flourishes the immunosuppressive and angiogenic tumor microenvironment in HCC. ( A–C ) Relative mRNA expression of the indicated genes in syngeneic subcutaneous tumors derived from Hep55.1c cells with NC or Car9 OE, measured by quantitative RT-PCR (NC: n=28; OE: n=25). Each dot represents one tumor; bars indicate mean±SEM. ( D ) UMAP of single-cell RNA sequencing data from NC and CA9 OE tumors, colored by annotated cell type (eg, malignant cells, T cells, TAMs, endothelial cells). ( E ) Frequency of CTLs per tumor sample, calculated as CTLs divided by total cells profiled by scRNA-seq (NC: n=3; CA9 OE: n=3). ( F, G ) Differential gene expression and representative cytotoxicity-related genes in CD8 + T cells from CA9 OE versus NC tumors. ( H, I ) Differential gene expression and representative TAM-related genes in TAMs from CA9 OE versus NC tumors. ( J–L ) Gene Set Enrichment Analysis (Gene Ontology) showed the top 20 pathways in TAMs ( J ), dendritic cells ( K ), and endothelial cells ( L ). ( M ) Tumor growth curves of syngeneic subcutaneous tumors derived from Car9-overexpressing Hep55.1c cells treated with vehicle, CA9 inhibitor alone, anti-PD-L1 plus anti-VEGF antibodies (Combi), or Combi plus CA9 inhibitor (Combi+CA9 inhibitor) (n=8–12 per group). Data are shown as mean±SEM. Group comparisons were performed using two-tailed unpaired Student’s t-tests or Wilcoxon rank-sum tests, as appropriate; p<0.05 was considered statistically significant. CAF, cancer-associated fibroblast; CA9, carbonic anhydrase 9; CTLs, cytotoxic T lymphocytes; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NC, negative control; NK, natural killer; OE, overexpression; PD-L1, programmed death-ligand 1; RT-PCR, reverse transcription PCR; scRNA-seq, single-cell RNA sequencing; TAM, tumor-associated macrophage; TAN, tumor-associated neutrophils; TPM, transcripts per million; UMAP, Uniform Manifold Approximation and Projection; VEGF, vascular endothelial growth factor; WT, wild type.

    Article Snippet: CA9 inhibitor S4 (MedChemExpress, Cat# HY-110243; 5 mg/kg, i.p.).

    Techniques: Expressing, Derivative Assay, Quantitative RT-PCR, Single Cell, RNA Sequencing, Gene Expression, Two Tailed Test, Negative Control, Over Expression, Reverse Transcription Polymerase Chain Reaction, Reverse Transcription