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Tocris cd39 inhibitor pom 1

Pharmacological inhibition of <t>CD39</t> combined with IL-2cx enhances antitumor CD8 + T cell response. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS <t>(gray),</t> <t>POM-1</t> (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1+ IL-2cx (blue). (A) Schematic representation of treatment protocol. (B) Tumor volumes measured on 7-15 d.p.i. Statistical analysis was performed on day 15 d.p.i. (C) Frequencies of T-I CD45 + leukocytes. (D) Frequencies of T-I CD8 + T cells. (E) Frequencies of T-I Ki-67 + CD8 + T cells. (F) Frequencies of T-I OVA-specific CD8 + T cells. (G) Representative contour plots and frequencies of GzmB + , CD107a + , Perforin +, or IFN-γ + total T-I CD8 + T cells. All data were collected on day 15 p.i. Results are representative of 4 independent experiments. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Cd39 Inhibitor Pom 1, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd39+inhibitor+pom+1/pmc12883794-55-1-4?v=Tocris
Average 95 stars, based on 81 article reviews

cd39 inhibitor pom 1 - by Bioz Stars, 2026-07

95/100 stars

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1) Product Images from "Targeting CD39 in combination with IL-2/anti-IL-2 complexes enhances cytotoxic immunity and limits tumor progression"

Article Title: Targeting CD39 in combination with IL-2/anti-IL-2 complexes enhances cytotoxic immunity and limits tumor progression

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2026.1730342

Pharmacological inhibition of CD39 combined with IL-2cx enhances antitumor CD8 + T cell response. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1+ IL-2cx (blue). (A) Schematic representation of treatment protocol. (B) Tumor volumes measured on 7-15 d.p.i. Statistical analysis was performed on day 15 d.p.i. (C) Frequencies of T-I CD45 + leukocytes. (D) Frequencies of T-I CD8 + T cells. (E) Frequencies of T-I Ki-67 + CD8 + T cells. (F) Frequencies of T-I OVA-specific CD8 + T cells. (G) Representative contour plots and frequencies of GzmB + , CD107a + , Perforin +, or IFN-γ + total T-I CD8 + T cells. All data were collected on day 15 p.i. Results are representative of 4 independent experiments. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Figure Legend Snippet: Pharmacological inhibition of CD39 combined with IL-2cx enhances antitumor CD8 + T cell response. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1+ IL-2cx (blue). (A) Schematic representation of treatment protocol. (B) Tumor volumes measured on 7-15 d.p.i. Statistical analysis was performed on day 15 d.p.i. (C) Frequencies of T-I CD45 + leukocytes. (D) Frequencies of T-I CD8 + T cells. (E) Frequencies of T-I Ki-67 + CD8 + T cells. (F) Frequencies of T-I OVA-specific CD8 + T cells. (G) Representative contour plots and frequencies of GzmB + , CD107a + , Perforin +, or IFN-γ + total T-I CD8 + T cells. All data were collected on day 15 p.i. Results are representative of 4 independent experiments. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Techniques Used: Inhibition, Injection

Treatment with POM-1 plus IL-2cx increased the frequency of PD-1 Int CD8 + T cells with cytotoxic potential. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of PD-1 Neg , PD-1 Int , and PD-1 High total T-I CD8 + T cells. (B) Frequencies of TOX- expressing (left) and TCF-1 + expressing (right) PD-1 Int total T-I CD8 + T cells. (C) Frequencies of Ki-67 + expressing PD-1 Int total T-I CD8 + T cells. (D) GzmB + , Perforin + , CD107a + , or IFN-γ + PD-1 Int total T-I CD8 + T cells. All data were collected on day 15 p.i. Data are presented as mean ± SD. Results are representative of 4 independent experiments. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Figure Legend Snippet: Treatment with POM-1 plus IL-2cx increased the frequency of PD-1 Int CD8 + T cells with cytotoxic potential. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of PD-1 Neg , PD-1 Int , and PD-1 High total T-I CD8 + T cells. (B) Frequencies of TOX- expressing (left) and TCF-1 + expressing (right) PD-1 Int total T-I CD8 + T cells. (C) Frequencies of Ki-67 + expressing PD-1 Int total T-I CD8 + T cells. (D) GzmB + , Perforin + , CD107a + , or IFN-γ + PD-1 Int total T-I CD8 + T cells. All data were collected on day 15 p.i. Data are presented as mean ± SD. Results are representative of 4 independent experiments. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Techniques Used: Injection, Expressing

CD39 inhibition combined with IL-2cx reshapes the immune landscape of the tumor microenvironment. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of T-I NK cells (left) and KLRG-1 + NK cells (right). (B) Frequencies of GzmA + , Perforin + , or CD107a + T-I NK cells. (C) Frequencies of T-I CD4 + conventional T cells (Tconv left) and Treg (right). (D) Frequencies of CD39 + cells within T-I Tconv cells. (E) Frequencies of GzmB + CD39 + Tconv cells. (F) Frequencies of T-I monocytic myeloid-derived suppressor cells (M-MDSC). (G) Frequencies of T-I CD39 + , CD38 + , or CD73 + expressing M-MDSCs. All data were collected on day 15 p.i. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Figure Legend Snippet: CD39 inhibition combined with IL-2cx reshapes the immune landscape of the tumor microenvironment. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of T-I NK cells (left) and KLRG-1 + NK cells (right). (B) Frequencies of GzmA + , Perforin + , or CD107a + T-I NK cells. (C) Frequencies of T-I CD4 + conventional T cells (Tconv left) and Treg (right). (D) Frequencies of CD39 + cells within T-I Tconv cells. (E) Frequencies of GzmB + CD39 + Tconv cells. (F) Frequencies of T-I monocytic myeloid-derived suppressor cells (M-MDSC). (G) Frequencies of T-I CD39 + , CD38 + , or CD73 + expressing M-MDSCs. All data were collected on day 15 p.i. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Techniques Used: Inhibition, Injection, Derivative Assay, Expressing

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Journal: Frontiers in Immunology

Article Title: Targeting CD39 in combination with IL-2/anti-IL-2 complexes enhances cytotoxic immunity and limits tumor progression

doi: 10.3389/fimmu.2026.1730342

Figure Lengend Snippet: Pharmacological inhibition of CD39 combined with IL-2cx enhances antitumor CD8 + T cell response. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1+ IL-2cx (blue). (A) Schematic representation of treatment protocol. (B) Tumor volumes measured on 7-15 d.p.i. Statistical analysis was performed on day 15 d.p.i. (C) Frequencies of T-I CD45 + leukocytes. (D) Frequencies of T-I CD8 + T cells. (E) Frequencies of T-I Ki-67 + CD8 + T cells. (F) Frequencies of T-I OVA-specific CD8 + T cells. (G) Representative contour plots and frequencies of GzmB + , CD107a + , Perforin +, or IFN-γ + total T-I CD8 + T cells. All data were collected on day 15 p.i. Results are representative of 4 independent experiments. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Article Snippet: The CD39 inhibitor POM-1 (TOCRIS) was injected i.p. in 200 μL PBS containing 250 μg of POM-1 on days 5, 7, 10, and 13 p.i.

Techniques: Inhibition, Injection

Journal: Frontiers in Immunology

Article Title: Targeting CD39 in combination with IL-2/anti-IL-2 complexes enhances cytotoxic immunity and limits tumor progression

doi: 10.3389/fimmu.2026.1730342

Figure Lengend Snippet: Treatment with POM-1 plus IL-2cx increased the frequency of PD-1 Int CD8 + T cells with cytotoxic potential. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of PD-1 Neg , PD-1 Int , and PD-1 High total T-I CD8 + T cells. (B) Frequencies of TOX- expressing (left) and TCF-1 + expressing (right) PD-1 Int total T-I CD8 + T cells. (C) Frequencies of Ki-67 + expressing PD-1 Int total T-I CD8 + T cells. (D) GzmB + , Perforin + , CD107a + , or IFN-γ + PD-1 Int total T-I CD8 + T cells. All data were collected on day 15 p.i. Data are presented as mean ± SD. Results are representative of 4 independent experiments. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Article Snippet: The CD39 inhibitor POM-1 (TOCRIS) was injected i.p. in 200 μL PBS containing 250 μg of POM-1 on days 5, 7, 10, and 13 p.i.

Techniques: Injection, Expressing

Journal: Frontiers in Immunology

Article Title: Targeting CD39 in combination with IL-2/anti-IL-2 complexes enhances cytotoxic immunity and limits tumor progression

doi: 10.3389/fimmu.2026.1730342

Figure Lengend Snippet: CD39 inhibition combined with IL-2cx reshapes the immune landscape of the tumor microenvironment. WT mice were injected s.c. with B16F10-OVA cells and treated with PBS (gray), POM-1 (red), IL-2/anti-IL-2 complex (IL-2cx, green), or the combination POM-1 + IL-2cx (blue). (A) Frequencies of T-I NK cells (left) and KLRG-1 + NK cells (right). (B) Frequencies of GzmA + , Perforin + , or CD107a + T-I NK cells. (C) Frequencies of T-I CD4 + conventional T cells (Tconv left) and Treg (right). (D) Frequencies of CD39 + cells within T-I Tconv cells. (E) Frequencies of GzmB + CD39 + Tconv cells. (F) Frequencies of T-I monocytic myeloid-derived suppressor cells (M-MDSC). (G) Frequencies of T-I CD39 + , CD38 + , or CD73 + expressing M-MDSCs. All data were collected on day 15 p.i. Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with multiple comparisons. Non-significant differences are not shown; * P ≤ 0.05; ** P ≤ 0.01; *** P ≤ 0.001; **** P ≤ 0.0001.

Article Snippet: The CD39 inhibitor POM-1 (TOCRIS) was injected i.p. in 200 μL PBS containing 250 μg of POM-1 on days 5, 7, 10, and 13 p.i.

Techniques: Inhibition, Injection, Derivative Assay, Expressing

Fig. 2 ATP (A), adenosine (B), and cAMP (C) levels in BALF following T/HS in the CD39, CD73, and A2BAR KO samples. ATP and cAMP were measured colorimetrically and adenosine was measured by a fluorometric assay. Data are mean ± S.D. (n = 4/ group) *p < 0.05 compared with T/SS-V, **p < 0.01 compared with T/ SS-V, #p < 0.05 compared with T/HS-V, ##p < 0.01 compared with T/ HS-V

Journal: Respiratory research

Article Title: Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering A 2B R signaling.

doi: 10.1186/s12931-023-02486-3

Figure Lengend Snippet: Fig. 2 ATP (A), adenosine (B), and cAMP (C) levels in BALF following T/HS in the CD39, CD73, and A2BAR KO samples. ATP and cAMP were measured colorimetrically and adenosine was measured by a fluorometric assay. Data are mean ± S.D. (n = 4/ group) *p < 0.05 compared with T/SS-V, **p < 0.01 compared with T/ SS-V, #p < 0.05 compared with T/HS-V, ##p < 0.01 compared with T/ HS-V

Article Snippet: The selective CD39 inhibitor sodium polyoxotungstate (POM1), CD73 inhibitor PSB 12,379 (N6-Benzyl-α,βmethyleneadenosine 5’-diphosphate disodium salt), and adenosine receptor agonist 1-(6-Amino-9 H-purin-9-yl)1-deoxy-N-ethyl-β-D-ribofuranuronamide (NECA) were from Tocris (Bristol, UK).

Techniques:

Fig. 1 T/HS increases CD39, CD73, and A2BAR expression in lung, liver, kidney, and gut. A–C CD39, CD73, and A2BAR expression were evaluated using western blotting of protein extracts. Data are mean ± S.D. (n = 4/group). **p < 0.01 compared with T/SS

Journal: Respiratory research

Article Title: Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering A 2B R signaling.

doi: 10.1186/s12931-023-02486-3

Figure Lengend Snippet: Fig. 1 T/HS increases CD39, CD73, and A2BAR expression in lung, liver, kidney, and gut. A–C CD39, CD73, and A2BAR expression were evaluated using western blotting of protein extracts. Data are mean ± S.D. (n = 4/group). **p < 0.01 compared with T/SS

Techniques: Expressing, Western Blot

Fig. 3 CD39, CD73, and A2BR regulation of lung permeability and MPO activity. Lung permeability was determined using the EBD method (A, C, E, G) and MPO activity as a surrogate for neutrophil sequestration (B, D, F, H) was determined spectrophotometrically. Data are mean ± S.D. (n = 4/ group). *p < 0.05 compared with corresponding T/SS, **p < 0.01 compared with corresponding T/SS, #p < 0.05 compared with corresponding T/HS-V, ##p < 0.01 compared with corresponding T/HS

Journal: Respiratory research

Article Title: Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering A 2B R signaling.

doi: 10.1186/s12931-023-02486-3

Figure Lengend Snippet: Fig. 3 CD39, CD73, and A2BR regulation of lung permeability and MPO activity. Lung permeability was determined using the EBD method (A, C, E, G) and MPO activity as a surrogate for neutrophil sequestration (B, D, F, H) was determined spectrophotometrically. Data are mean ± S.D. (n = 4/ group). *p < 0.05 compared with corresponding T/SS, **p < 0.01 compared with corresponding T/SS, #p < 0.05 compared with corresponding T/HS-V, ##p < 0.01 compared with corresponding T/HS

Techniques: Permeability, Activity Assay

Fig. 4 Effect of NECA on lung MPO activity in CD39−/− and CD73−/− mice. MPO activity was determined from the lung spectrophotometrically (A, B). Data are mean ± S.D. (n = 4/group). *p < 0.05 compared with T/HS, **p < 0.05 compared with T/HS

Journal: Respiratory research

Article Title: Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering A 2B R signaling.

doi: 10.1186/s12931-023-02486-3

Figure Lengend Snippet: Fig. 4 Effect of NECA on lung MPO activity in CD39−/− and CD73−/− mice. MPO activity was determined from the lung spectrophotometrically (A, B). Data are mean ± S.D. (n = 4/group). *p < 0.05 compared with T/HS, **p < 0.05 compared with T/HS

Techniques: Activity Assay

FIGURE 1 Phenotype of gingiva‐derived mesenchymal stem cells (GMSCs). The following ﬂuorescent dye‐conjugated mouse anti‐human anti- bodies were used: anti‐CD90, anti‐CD29, anti‐CD44, anti‐CD73, anti‐CD105, anti‐CD39, anti‐CD4, anti‐CD34, anti‐CD45, anti‐CD14, and anti‐CD11b. GMSCs and human dermal ﬁbroblasts were stained with these monoclonal antibodies and analyzed by ﬂow cytometry. Data indicate the mean ± SEM of two independent experiments (n = 6 each group). Data were analyzed using the Mann–Whitney test for comparisons between two groups (**P < 0.01). NS, not signiﬁcant; SEM, standard error of the mean.

Journal: Rheumatology & Autoimmunity

Article Title: Human gingival tissue‐derived mesenchymal stem cells inhibit proliferation and invasion of rheumatoid fibroblast‐like synoviocytes via the CD39/CD73 signaling pathway

doi: 10.1002/rai2.12075

Figure Lengend Snippet: FIGURE 1 Phenotype of gingiva‐derived mesenchymal stem cells (GMSCs). The following ﬂuorescent dye‐conjugated mouse anti‐human anti- bodies were used: anti‐CD90, anti‐CD29, anti‐CD44, anti‐CD73, anti‐CD105, anti‐CD39, anti‐CD4, anti‐CD34, anti‐CD45, anti‐CD14, and anti‐CD11b. GMSCs and human dermal ﬁbroblasts were stained with these monoclonal antibodies and analyzed by ﬂow cytometry. Data indicate the mean ± SEM of two independent experiments (n = 6 each group). Data were analyzed using the Mann–Whitney test for comparisons between two groups (**P < 0.01). NS, not signiﬁcant; SEM, standard error of the mean.

Article Snippet: A CD39 inhibitor (sodium polyoxotungstate, POM1) was supplied by Tocris Bioscience (Bristol, UK).

Techniques: Derivative Assay, Staining, Bioprocessing, Cytometry, MANN-WHITNEY

FIGURE 3 GMSCs suppress the proliferation of RA FLSs via CD39/CD73 signaling. GMSCs (0, 1, 10, and 20 × 103) or human dermal ﬁbroblast (20 × 103) were seeded in each well for 24 h. RA FLSs were starved for 24 h and then cultured in the presence of PDGF (20 ng/mL) with or without GMSCs or human dermal ﬁbroblasts for 72 h. Hoechst 33342 (blue, upper panel) and 5‐ethynyl‐2‐deoxyuridine (EdU) (red, middle panel) staining, and merged images (lower panel) are shown. Image‐Pro Plus software was used for analysis. The number of positive cells was counted in ﬁve random visual ﬁelds at a ×200 magniﬁcation, and then the average was calculated as the number of positive cells. Representative images (A) and summarized data (B) of three independent experiments (n = 6) are shown. (C) GMSCs were pretreated with IDOi, CD39i, or CD73i to explore the mechanism. Data indicate the mean ± SEM of three independent experiments (six RA FLS lines). Control: no GMSCs; **P < 0.01. GMSCs, gingiva‐derived mesenchymal stem cells; NS, not signiﬁcant; PDGF, platelet‐derived growth factor; RA FLSs, rheumatoid arthritis ﬁbroblast‐ like synoviocytes; SEM, standard error of the mean.

Journal: Rheumatology & Autoimmunity

Article Title: Human gingival tissue‐derived mesenchymal stem cells inhibit proliferation and invasion of rheumatoid fibroblast‐like synoviocytes via the CD39/CD73 signaling pathway

doi: 10.1002/rai2.12075

Figure Lengend Snippet: FIGURE 3 GMSCs suppress the proliferation of RA FLSs via CD39/CD73 signaling. GMSCs (0, 1, 10, and 20 × 103) or human dermal ﬁbroblast (20 × 103) were seeded in each well for 24 h. RA FLSs were starved for 24 h and then cultured in the presence of PDGF (20 ng/mL) with or without GMSCs or human dermal ﬁbroblasts for 72 h. Hoechst 33342 (blue, upper panel) and 5‐ethynyl‐2‐deoxyuridine (EdU) (red, middle panel) staining, and merged images (lower panel) are shown. Image‐Pro Plus software was used for analysis. The number of positive cells was counted in ﬁve random visual ﬁelds at a ×200 magniﬁcation, and then the average was calculated as the number of positive cells. Representative images (A) and summarized data (B) of three independent experiments (n = 6) are shown. (C) GMSCs were pretreated with IDOi, CD39i, or CD73i to explore the mechanism. Data indicate the mean ± SEM of three independent experiments (six RA FLS lines). Control: no GMSCs; **P < 0.01. GMSCs, gingiva‐derived mesenchymal stem cells; NS, not signiﬁcant; PDGF, platelet‐derived growth factor; RA FLSs, rheumatoid arthritis ﬁbroblast‐ like synoviocytes; SEM, standard error of the mean.

Article Snippet: A CD39 inhibitor (sodium polyoxotungstate, POM1) was supplied by Tocris Bioscience (Bristol, UK).

Techniques: Cell Culture, Staining, Software, Control, Derivative Assay

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