adenosine a2a receptor a2ar antagonist sch58261  (MedChemExpress)

Journal: Bioactive Materials

Article Title: Immunomodulatory supramolecular hydrogel for rheumatoid arthritis management via adenosine A2A receptor-mediated macrophage remodeling

doi: 10.1016/j.bioactmat.2025.11.031

Figure Lengend Snippet: The design of an inflammatory macrophages-targeted, acid-sensitive PNSH for delivery MTX and its role in promoting A2AR activation on M2 macrophages for arthritis therapy. (A)The structure of acid-sensitive polymer-nanomedicine supramolecular hydrogels, composed of drug-loaded MTX NPs. (B) Schematic illustration of arthritis therapy targeting inflammatory joint network via mPECN NPs-mediated release of MTX. This approach leverages MTX targeting the A2AR and repolarization of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Activation of A2AR and macrophage repolarization by mPECN-MTX NPs synergistically enhanced the anti-inflammatory effect of PNSH-mediated nanomedicine in an arthritis rat model.

Article Snippet: The selective adenosine A2A receptor (A2AR) antagonist SCH58261 (HY-19533) was purchased from MedChemExpress (Shanghai, China).

Techniques: Activation Assay, Polymer

Journal: Bioactive Materials

Article Title: Immunomodulatory supramolecular hydrogel for rheumatoid arthritis management via adenosine A2A receptor-mediated macrophage remodeling

doi: 10.1016/j.bioactmat.2025.11.031

Figure Lengend Snippet: MTX@PNSH promotes anti-inflammatory M2 macrophages through the A2AR signaling pathway. (A) The intracellular cAMP levels in Raw 264.7 cells were determined by homogeneous time-resolved fluorescence (HTRF) following different treatments. (B) qRT-PCR analysis of relative mRNA of A2ar with different treatments. (C) Immunostaining of A2AR expression in Raw 264.7 cells with different treatments. (D) Flow cytometry analysis of A2AR + cells in Raw 264.7 cells with different treatments and the percentage of A2AR + cells in Raw 264.7 cells with different treatments. (E) qRT-PCR analysis of relative mRNA expression of Pdl1 without LPS treatment. (F) qRT-PCR analysis of relative mRNA expression of Ido1 without LPS treatment. (G) qRT-PCR analysis of relative mRNA expression of Pdl1 with LPS treatment. (H) qRT-PCR analysis of relative mRNA expression of Ido1 with LPS treatments. (I) Western blotting analysis of A2AR protein level in macrophages after 24 h of different treatment with or without A2AR inhibitor. (J) Quantitative analysis of A2AR protein level in different treatments with or without A2AR inhibitor. (K) Flow cytometry analysis of CD11b and CD39 in Raw 264.7 cells with different treatments and the percentage of CD11b + CD39 + macrophages. (L) Flow cytometry analysis of CD11b and CD73 in Raw 264.7 cells with different treatments and the percentage of CD11b + CD73 + macrophages. (M) Flow cytometry analysis of CD11b and PD-L1 in Raw 264.7 cells after 24 h of different treatments and the percentage of CD11b + PD-L1 + macrophages in Raw 264.7 cells after 24 h of different treatments. Data are presented as mean ± SD, n = 3. Statistical significance was determined using one-way ANOVA, followed by Dunnett's post hoc test for comparisons between groups.

Article Snippet: The selective adenosine A2A receptor (A2AR) antagonist SCH58261 (HY-19533) was purchased from MedChemExpress (Shanghai, China).

Techniques: Fluorescence, Quantitative RT-PCR, Immunostaining, Expressing, Flow Cytometry, Western Blot

Journal: Drug Design, Development and Therapy

Article Title: Cordycepin Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Inhibiting IL-6/IL-6R-Mediated p38 MAPK and NF-κB Activation Through Adenosine A 2A Receptor Stimulation

doi: 10.2147/DDDT.S575035

Figure Lengend Snippet: Cordycepin abates DSS-induced damage in NCM460 cells by activating adenosine receptor A 2A . ( A ) The cAMP levels in NCM460 cells under treatment with 2% DSS and/or 1 μmol/L and 10 μmol/L COR. ( B ) The cAMP levels in NCM460 cells under treatment with 2% DSS, 10 μmol/L COR, 5 μmol/L SCH58261 (SCH), and / or 5 μmol/L DPCPX for 24 h. The release levels of ( C ) LDH, ( D ) IL-1β, ( E ) IL-6, and ( F ) TNF-α were measured by using Elisa. ( G ) Representative images of PI staining and the percentage of PI-positive cells, scar bar = 100 μm. ( H – J ) The protein expression of ZO-1, A 2A AR and A 1 AR in NCM460 cells was determined by using Western blotting assay. The results were representative of three independent experiments and expressed as mean ± SEM. Data were compared using two-tailed Student’s t tests. vs. control group; # P < 0.05, vs. control group; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the 2% DSS group.

Article Snippet: Cordycepin (COR, CAS No. 73–03-0, Cat. No. C805132, 98% purity) was purchased from Shanghai Macklin Biochemical Technology Co., Ltd. (China); Dextran Sodium Sulfate (DSS, 60316ES60) was provided by Yeasen Biotechnology Co., Ltd. (Shanghai, China); Sulfasalazine (SASP, S129986) was obtained from Shanghai Aladdin Biochemical Technology Co., Ltd. (China); SCH58261 (HY-19533) and DPCPX (HY-100937) were supplied by MedChemExpress (MCE, Monmouth Junction, NJ, USA); BisBenzimide H 33342 (Hoechst 33342, C0030), and Propidium Iodide (PI, C0080) were purchased from Beijing Solarbio Science & Technology Co., Ltd. Proteintech Co., Ltd. (Wuhan, China), supplied the antibody against Zonula Occludens-1 (ZO-1, 21,773-1-AP), Occludin Polyclonal antibody (27260-1-AP), Adenosine A 1 receptor Polyclonal antibody (A 1 AR, 20332-1-AP), the antibody against β-actin (20536-1-AP), CD126/IL-6R alpha Polyclonal antibody (23457-1-AP), Horseradish peroxidase (HRP)-conjugated goat anti-rabbit secondary antibody (SA00001-2), and HRP-conjugated goat anti-mouse secondary antibody (SA00001-1).

Techniques: Enzyme-linked Immunosorbent Assay, Staining, Expressing, Western Blot, Two Tailed Test, Control

Journal: Drug Design, Development and Therapy

Article Title: Cordycepin Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Inhibiting IL-6/IL-6R-Mediated p38 MAPK and NF-κB Activation Through Adenosine A 2A Receptor Stimulation

doi: 10.2147/DDDT.S575035

Figure Lengend Snippet: SCH58261 blocks cordycepin’s ameliorative effects on DSS-induced acute colitis symptoms in mice. ( A ) Animal experimental flowchart. ( B ) The body weight change. ( C ) The disease activity index (DAI). ( D ) The colon length. ( E – I ) Serum level of TNF-α, IL-1β, IL-6, IFN-γ and CRP. ( J ) The histopathological damage of colons was detected by using H&E staining. ( K ) Histological score. Data were presented as the means ± SEM of six-eight mice in each group and were compared using two-tailed Student’s t tests. ## P < 0.01, ### P < 0.001 and #### P < 0.0001 vs. control group; *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 vs. the DSS model (DSS) group.

Article Snippet: Cordycepin (COR, CAS No. 73–03-0, Cat. No. C805132, 98% purity) was purchased from Shanghai Macklin Biochemical Technology Co., Ltd. (China); Dextran Sodium Sulfate (DSS, 60316ES60) was provided by Yeasen Biotechnology Co., Ltd. (Shanghai, China); Sulfasalazine (SASP, S129986) was obtained from Shanghai Aladdin Biochemical Technology Co., Ltd. (China); SCH58261 (HY-19533) and DPCPX (HY-100937) were supplied by MedChemExpress (MCE, Monmouth Junction, NJ, USA); BisBenzimide H 33342 (Hoechst 33342, C0030), and Propidium Iodide (PI, C0080) were purchased from Beijing Solarbio Science & Technology Co., Ltd. Proteintech Co., Ltd. (Wuhan, China), supplied the antibody against Zonula Occludens-1 (ZO-1, 21,773-1-AP), Occludin Polyclonal antibody (27260-1-AP), Adenosine A 1 receptor Polyclonal antibody (A 1 AR, 20332-1-AP), the antibody against β-actin (20536-1-AP), CD126/IL-6R alpha Polyclonal antibody (23457-1-AP), Horseradish peroxidase (HRP)-conjugated goat anti-rabbit secondary antibody (SA00001-2), and HRP-conjugated goat anti-mouse secondary antibody (SA00001-1).

Techniques: Activity Assay, Staining, Two Tailed Test, Control

Journal: Drug Design, Development and Therapy

Article Title: Cordycepin Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice by Inhibiting IL-6/IL-6R-Mediated p38 MAPK and NF-κB Activation Through Adenosine A 2A Receptor Stimulation

doi: 10.2147/DDDT.S575035

Figure Lengend Snippet: SCH58261 blocks cordycepin’s amelioration of intestinal inflammation and gut barrier function in DSS-induced colitis mice. ( A – C ) Level of colonic IL-1β, IL-6, and TNF-α among the Control, DSS, DSS+COR-L and DSS+COR-H group were detected by using Elisa. ( D ) Representative images of AB-PAS staining of colonic tissue. The arrow indicates the goblet cells. ( E ) Number of goblet cells in colonic tissue. ( F ) Representative images of TUNEL staining in colonic tissue, scale bar = 50 μm. ( G ) Percentage of TUNEL-positive cells (%). ( H ) The protein expression of ZO-1 and Occludin in colons was determined by using Western blotting assay. ( I ) and ( J ) Serum level of D-lactate and diamine oxidase (DAO) were measured by using Elisa. ( K ) The serum cAMP levels among the control, DSS, DSS+COR-L, DSS+COR-H group and DSS+SCH+COR-H group. Data were presented as the means ± SEM of six-eight mice in each group and were compared using two-tailed Student’s t tests. # P < 0.05, ## P < 0.01, ### P < 0.001 and #### P < 0.0001 vs. control group; *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 vs. the DSS model (DSS) group.

Article Snippet: Cordycepin (COR, CAS No. 73–03-0, Cat. No. C805132, 98% purity) was purchased from Shanghai Macklin Biochemical Technology Co., Ltd. (China); Dextran Sodium Sulfate (DSS, 60316ES60) was provided by Yeasen Biotechnology Co., Ltd. (Shanghai, China); Sulfasalazine (SASP, S129986) was obtained from Shanghai Aladdin Biochemical Technology Co., Ltd. (China); SCH58261 (HY-19533) and DPCPX (HY-100937) were supplied by MedChemExpress (MCE, Monmouth Junction, NJ, USA); BisBenzimide H 33342 (Hoechst 33342, C0030), and Propidium Iodide (PI, C0080) were purchased from Beijing Solarbio Science & Technology Co., Ltd. Proteintech Co., Ltd. (Wuhan, China), supplied the antibody against Zonula Occludens-1 (ZO-1, 21,773-1-AP), Occludin Polyclonal antibody (27260-1-AP), Adenosine A 1 receptor Polyclonal antibody (A 1 AR, 20332-1-AP), the antibody against β-actin (20536-1-AP), CD126/IL-6R alpha Polyclonal antibody (23457-1-AP), Horseradish peroxidase (HRP)-conjugated goat anti-rabbit secondary antibody (SA00001-2), and HRP-conjugated goat anti-mouse secondary antibody (SA00001-1).

Techniques: Control, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Expressing, Western Blot, Two Tailed Test

Journal: Animal Nutrition

Article Title: Ruminal microbiota-derived inosine alleviates metabolic disorders in dairy cows supplemented with grape seed extract

doi: 10.1016/j.aninu.2025.04.009

Figure Lengend Snippet: Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.

Article Snippet: To determine the biologically-active inosine receptor type in hepatocyte metabolism, hepatocytes were separately pretreated with: 1) 100 nmol/L A1R inhibitor derenofylline (SLV320, Cat. # HY-14858, MedChemExpress, Shanghai, China); 2) 1 μmol/L A2aR inhibitor ( SCH58261 , Cat. # HY-19533, MedChemExpress); 3) siRNA against A2bR or A3R.

Techniques: Staining, Control, Western Blot, Transfection, Small Interfering RNA, Binding Assay, Phospho-proteomics

Journal: Animal Nutrition

Article Title: Ruminal microbiota-derived inosine alleviates metabolic disorders in dairy cows supplemented with grape seed extract

doi: 10.1016/j.aninu.2025.04.009

Figure Lengend Snippet: Inosine inhibited lipolysis and inflammation in bovine adipocytes. (A and B) Triglyceride content in adipocytes and glycerol content in the supernatant. Cells were treated with 0, 1, 2, 5 and 10 μmol/L inosine for 12 h after 10 μmol/L ISO pre-treatment for 3 h. (C-E) Western blotting of p-HSL/HSL and ATGL. Adipocytes were treated with 1 μmol/L inosine for 12 h after pre-treatment with ISO for 3 h. (F–H) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with 1 μmol/L inosine, 1 μg/mL LPS or co-treatment for 12 h. (I and J) Triglyceride content in adipocytes and glycerol content in supernatant. Adipocytes were pre-treated with 10 μmol/L ISO for 3 h, and then treated with 1 μmol/L inosine for 12 h after 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) treatment for 30 min or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor). (K-M) Western blotting of p-HSL/HSL and ATGL. Adipocytes were pre-treated with ISO for 3 h, and then treated with inosine for 12 h after SLV320 treatment for 30 min. (N–P) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with inosine and LPS for 12 h, after SLV320 treatment for 30 min. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). ISO = isoprenaline hydrochloride; HSL = hormone-sensitive lipase; p-HSL = phosphorylation of HSL; ATGL = adipose triglyceride lipase; NF-κB = nuclear factor kappa B; p–NF–κB = phosphorylation of NF-κB; IκBα = NF-κB inhibitor alpha; p-IκBα = phosphorylation of IκBα; LPS = lipopolysaccharide.

Article Snippet: To determine the biologically-active inosine receptor type in hepatocyte metabolism, hepatocytes were separately pretreated with: 1) 100 nmol/L A1R inhibitor derenofylline (SLV320, Cat. # HY-14858, MedChemExpress, Shanghai, China); 2) 1 μmol/L A2aR inhibitor ( SCH58261 , Cat. # HY-19533, MedChemExpress); 3) siRNA against A2bR or A3R.

Techniques: Western Blot, Transfection, Small Interfering RNA, Phospho-proteomics

Journal: bioRxiv

Article Title: Glutamine-Dependent Biosynthetic Pathways Fuel Autoreactive T and B Cells in Foxp3 Deficiency-mediated Disease

doi: 10.1101/2025.11.04.686569

Figure Lengend Snippet: A-I, Representative flow cytometric analysis and frequencies (scatter plots and means) of ΔTreg (CD90 + CD4 + CD8 − YFP + ) cells ( A,B ), CD62L lo CD44 hi , CD62L hi CD44 lo CD4 + Tconv (CD90 + CD4 + CD8 − YFP − ) cells ( C,D ), IFN-γ and IL-4 expression by CD4 + Tconv cells ( E,F ), IgG1 + IgD − B (CD19 + ) cells ( G,H ), GL-7 + CD38 − germinal center B cells ( I ) from the spleen of mice treated with vehicle, DON, DON+ASN or DON+SCH58261. J , Heatmap of IgG reactivity to auto-antigen array analysis in the serum of untreated age-matched WT and Foxp3 ΔEGFPiCre R26 YFP mice treated with vehicle, DON or DON+ASN. Fold change values for each group were calculated by normalizing with the values of WT mice. The observed fold change values are color-coded per the legend immediately to the top of the heatmap. K , Serum concentrations of immunoglobulin IgM, IgA, IgG1, IgG2b, IgG2c, IgG3 and IgE of mice of the respective treatment. L , M , Representative immunofluorescence pictures of IgG deposit (original magnification; ×200; ( L ) and mean florescent intensity ( M ) of kidney of mice of the respective treatment. (n = 6). N,O , Representative microscopic pictures of H&E staining (original magnification; ×200; ( N ) and histological scores ( O ) of the skin and kidney of mice of the respective treatment (n = 9). Statistical significance was determined by one-way ANOVA with Tukey’s multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001.

Article Snippet: SCH58261 was purchased from Tocris (#Catalog 2270).

Techniques: Expressing, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: A CT26 CRC cells were stained with PKH26GL (red) and quinacrine (green) fluorescent dyes. Images were acquired using confocal microscopy at time 0 and after 5 min following P2X7 activation with 300 µM BzATP and are extrapolated from a 30-min time course (see supplementary videos and ). B CT26 cells were pre-treated with P2X7 antagonist AZ10606120 (5 µM) for 10 min before application of BzATP. C Number of vesicles released in 30 min from CT26 cells in PBS vehicle (PBS S-VS), following stimulation with P2X7 agonist ATP (P2X7-VS) or 10 min pretreatment with P2X7 antagonist AZ10606120 followed by stimulation with 3 mM ATP (AZ-VS) ( n = 5). D Size of PBS S-VS, P2X7-VS, and AZ-VS ( n = 5). E Number of vesicles released in 30 min from CT26 cells in DMSO vehicle (DMSO S-VS), following stimulation with P2X7 agonist ATP (P2X7-VS) or 10 min pretreatment with P2X7 antagonist A740003 followed by stimulation with 3 mM ATP (A74-VS) ( n = 7). F Size of DMSO- S-VS, P2X7-VS, and A74-VS ( n = 7). G Western blot for GM130, Alix, P2X7, CD39, CD73, and A2A in CT26 cells, S-VS and P2X7-VS. Pericellular ATP was measured with the pmeLUC probe expressed on the cell surface of untreated CT26 cells or after 5 min of exposure to PBS vehicle, S-VS, and P2X7-VS ( n = 4). H Quantification of luminescence changes was expressed as a fold increase on time 0. I Representative images of photon emissions. Changes in ATP J concentration increase on time 0 in the supernatants of CT26 cells, untreated or treated with PBS vehicle, S-VS, or P2X7-VS, measured with a luciferin/luciferase assay ( n = 3). Changes in adenosine K concentration increase on time 0 in the supernatants of CT26 cells untreated or treated with PBS vehicle, S-VS, P2X7-VS, or P2X7-VS plus 5uM CD73 inhibitor AB680 ( n = 5). * p < 0.05, ** p < 0.001, *** p < 0,0001, **** p < 0.00001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Staining, Confocal Microscopy, Activation Assay, Western Blot, Concentration Assay, Luciferase

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: Percentage of lung cells positive to P2X7 A and A2A F staining in mice injected intravenously with only CT26 Luc2 cells or CT26 Luc2 pre-treated with S-VS, P2X7-VS, and AZ-VS ( n = 3). Representative immunohistochemistry images of mice injected intravenously with CT26 Luc2 alone B , G or pre-treated with S-VS C , H , P2X7-VS D , I , or AZ-VS E , J . * p < 0.05, ** p < 0.001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Staining, Injection, Immunohistochemistry

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: Mice were injected intravenously with CT26 Luc2 cells and treated intraperitoneally with placebo, the P2X7 antagonist AZ10606120 (2 mg/Kg), the A2A antagonist SCH58261 (1 mg/Kg), or both drugs every three days. A Quantification of photon emission, expressed as total flux (p/s), on day 14 from the inoculum ( n = 6) B Representative images of photon emission at day 14 from the inoculum. C Area of metastasis expressed as a percentage of total lung area ( n = 6). Representative hematoxylin/eosin staining of lungs from mice treated with D placebo, E the P2X7 antagonist AZ10606120 (2 mg/Kg), F the A2A antagonist SCH58261 (1 mg/Kg), and G combination of the two drugs. Black arrows indicate metastatic lesions. Systemic levels of H IL-17 ( n = 6) and I IL-23 ( n = 4) were measured in the plasma of tumor-bearing mice. Systemic levels of J IL-17 ( n = 4) and K IL-23 ( n = 4) measured in the plasma of mice not injected with tumor cells but treated only with placebo, AZ10606120 (2 mg/Kg), SCH58261 (1 mg/Kg), or both compounds.* p < 0.05, ** p < 0.001, *** p < 0.0001, **** p < 0.00001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Injection, Staining, Clinical Proteomics

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: A–J BALB/c mice were injected intravenously with CT26 Luc2 cells and treated intraperitoneally with placebo, AZ10606120 (2 mg/Kg), SCH58261 (1 mg/Kg), or a combination of both drugs. Percentage of lung cells positive for P2X7 A and A2A F staining ( n = 4). Representative immunohistochemistry images of mice treated with placebo B , G , P2X7 antagonist AZ10606120 (C, H), A2A antagonist SCH58261 D , I , or both drugs E , J . * p < 0.05.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Injection, Staining, Immunohistochemistry

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: BALB/c mice were subcutaneously injected with CT26 and treated with placebo, AZ10606120 (2 mg/Kg), SCH58261 (1 mg/Kg) or both drugs ( n = 12). A Ex vivo tumor volume on day 14, and B representative images of tumors. C Systemic levels of the proinflammatory cytokine IL-17 ( n = 4). nude/nude mice were subcutaneously injected with HCT116 cells and treated i.p. with placebo, AZ10606120 (2 mg/Kg), SCH58261 (1 mg/Kg) or both drugs. D Ex vivo tumor volume at day 14 from the inoculum ( n = 6). E Representative tumor image. F HCT116 Luc2 were injected into the tail vein of nude/nude mice and treated with placebo, AZ10606120 (2 mg/Kg), SCH58261 (1 mg/Kg) or both drugs ( n = 7). Photon emission on day 14 total flux (p/s). G Image representative of data shown in F . * p < 0.05, ** p < 0.001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Injection, Ex Vivo

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: The mRNA expression of P2X7A A , B , P2X7B C , D , CD39 E , F , CD73 G , H , and A2A I , J was evaluated in the cDNAs of 158 patients with CRC subdivided into stage I ( n = 24), stage II ( n = 50), stage III ( n = 52), and stage IV ( n = 32) which comprised 11 samples derived from metastases in organs other than the colon. K Spearman’s correlation coefficient among P2X7A, P2X7B, CD39, CD73 , and A2A was evaluated in CRC metastatic patients. L Spearman’s correlation coefficient was evaluated between P2X7 and A2A expression in colon adenocarcinoma samples obtained from the Cancer Genome Atlas database. * p < 0.05, ** p < 0.01, *** p < 0.001. **** p < 0.0001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Expressing, Derivative Assay

Journal: Cell Death & Disease

Article Title: P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis

doi: 10.1038/s41419-025-07897-2

Figure Lengend Snippet: mRNA expression of A P2X7A , B P2X7B , C A2A , D CD39 , and E CD73 in CRC patients subdivided into APC WT and APC mutated groups ( n = 6). Percentage of cells positive for P2X7 F and A2A G in the colons of WT and PIRC rats and PIRC tumors ( n = 4). Representative images of immunohistochemical staining for P2X7 and A2A in the colon of WT 1-year rats H, K and in the normal colon I, L and the tumor mass J, M of 1-year PIRC rats. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: After five days, when tumor masses became evident, we started the treatment, which was repeated every 72 h, with an intraperitoneal (i.p.) injection of placebo (PBS + 0.002% DMSO), the P2X7 antagonist AZ10606120 (2 mg/Kg) (Tocris Bioscience), the A2A antagonist SCH58261 (1 mg/Kg) (Tocris Bioscience), and a combination of both antagonists.

Techniques: Expressing, Immunohistochemical staining, Staining