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Preclinical efficacy and antitumor activity of CTX130. A, Proliferation of CTX130 versus CD70 + CAR T cells. B, CTX130 and CD70 + anti-CD70 CAR T-cell cytotoxicity as a percentage of cell lysis after repeated challenges with CD70 + <t>A498</t> cells. Data points represent a single measurement. C, CTX130 cytotoxicity toward CD70 high (A498), CD70 low (ACHN), and CD70 − (MCF7) cell lines. Results from cells treated with CTX130 are shown with solid circles, and results from cells treated with unedited T cells are shown with open squares. The graph shows the mean ± SD from 3 technical replicates with increasing ratios of CTX130 or unedited T cells to tumor cells (0.125:1 to 4:1). D, Antitumor activity of CAR T cells in an RCC xenograft model. Mice were either left untreated ( n = 5) or injected with CTX130 ( n = 5) or CD70 + anti-CD70 CAR T cells ( n = 4). Each point represents the mean tumor volume ± SEM. E, Disruption of the PD-1 checkpoint gene is detrimental to CTX130 CAR T-cell function in a xenograft rechallenge model. Following the first injection of tumor cells, mice ( n = 5 per group) were left untreated (open circles) or treated with CTX130 (open squares) or PD1 − CTX130 CAR T cells (open triangles). At the day 25 rechallenge, fresh tumor cells were injected into the left flank of treated mice (CTX130-treated and PD1 − CTX130-treated animals represented by solid circles and solid triangles, respectively) and a new control group (open lozenges). Each point represents the mean tumor volume ± SEM. F, Mortality due to GvHD in mice ( n = 30 per group) treated with unedited T cells or low (20 million cells/mouse) or high (40 million cells/mouse) doses of CTX130. CAR, chimeric antigen receptor; CD, cluster of differentiation; EP, electroporation; GvHD, graft versus host disease; KO, knockout; PD-1, programmed cell death 1; RCC, renal cell carcinoma.
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Preclinical efficacy and antitumor activity of CTX130. A, Proliferation of CTX130 versus CD70 + CAR T cells. B, CTX130 and CD70 + anti-CD70 CAR T-cell cytotoxicity as a percentage of cell lysis after repeated challenges with CD70 + <t>A498</t> cells. Data points represent a single measurement. C, CTX130 cytotoxicity toward CD70 high (A498), CD70 low (ACHN), and CD70 − (MCF7) cell lines. Results from cells treated with CTX130 are shown with solid circles, and results from cells treated with unedited T cells are shown with open squares. The graph shows the mean ± SD from 3 technical replicates with increasing ratios of CTX130 or unedited T cells to tumor cells (0.125:1 to 4:1). D, Antitumor activity of CAR T cells in an RCC xenograft model. Mice were either left untreated ( n = 5) or injected with CTX130 ( n = 5) or CD70 + anti-CD70 CAR T cells ( n = 4). Each point represents the mean tumor volume ± SEM. E, Disruption of the PD-1 checkpoint gene is detrimental to CTX130 CAR T-cell function in a xenograft rechallenge model. Following the first injection of tumor cells, mice ( n = 5 per group) were left untreated (open circles) or treated with CTX130 (open squares) or PD1 − CTX130 CAR T cells (open triangles). At the day 25 rechallenge, fresh tumor cells were injected into the left flank of treated mice (CTX130-treated and PD1 − CTX130-treated animals represented by solid circles and solid triangles, respectively) and a new control group (open lozenges). Each point represents the mean tumor volume ± SEM. F, Mortality due to GvHD in mice ( n = 30 per group) treated with unedited T cells or low (20 million cells/mouse) or high (40 million cells/mouse) doses of CTX130. CAR, chimeric antigen receptor; CD, cluster of differentiation; EP, electroporation; GvHD, graft versus host disease; KO, knockout; PD-1, programmed cell death 1; RCC, renal cell carcinoma.
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Preclinical efficacy and antitumor activity of CTX130. A, Proliferation of CTX130 versus CD70 + CAR T cells. B, CTX130 and CD70 + anti-CD70 CAR T-cell cytotoxicity as a percentage of cell lysis after repeated challenges with CD70 + A498 cells. Data points represent a single measurement. C, CTX130 cytotoxicity toward CD70 high (A498), CD70 low (ACHN), and CD70 − (MCF7) cell lines. Results from cells treated with CTX130 are shown with solid circles, and results from cells treated with unedited T cells are shown with open squares. The graph shows the mean ± SD from 3 technical replicates with increasing ratios of CTX130 or unedited T cells to tumor cells (0.125:1 to 4:1). D, Antitumor activity of CAR T cells in an RCC xenograft model. Mice were either left untreated ( n = 5) or injected with CTX130 ( n = 5) or CD70 + anti-CD70 CAR T cells ( n = 4). Each point represents the mean tumor volume ± SEM. E, Disruption of the PD-1 checkpoint gene is detrimental to CTX130 CAR T-cell function in a xenograft rechallenge model. Following the first injection of tumor cells, mice ( n = 5 per group) were left untreated (open circles) or treated with CTX130 (open squares) or PD1 − CTX130 CAR T cells (open triangles). At the day 25 rechallenge, fresh tumor cells were injected into the left flank of treated mice (CTX130-treated and PD1 − CTX130-treated animals represented by solid circles and solid triangles, respectively) and a new control group (open lozenges). Each point represents the mean tumor volume ± SEM. F, Mortality due to GvHD in mice ( n = 30 per group) treated with unedited T cells or low (20 million cells/mouse) or high (40 million cells/mouse) doses of CTX130. CAR, chimeric antigen receptor; CD, cluster of differentiation; EP, electroporation; GvHD, graft versus host disease; KO, knockout; PD-1, programmed cell death 1; RCC, renal cell carcinoma.

Journal: Cancer Discovery

Article Title: CD70-Targeted Allogeneic CAR T-Cell Therapy for Advanced Clear Cell Renal Cell Carcinoma

doi: 10.1158/2159-8290.CD-24-0102

Figure Lengend Snippet: Preclinical efficacy and antitumor activity of CTX130. A, Proliferation of CTX130 versus CD70 + CAR T cells. B, CTX130 and CD70 + anti-CD70 CAR T-cell cytotoxicity as a percentage of cell lysis after repeated challenges with CD70 + A498 cells. Data points represent a single measurement. C, CTX130 cytotoxicity toward CD70 high (A498), CD70 low (ACHN), and CD70 − (MCF7) cell lines. Results from cells treated with CTX130 are shown with solid circles, and results from cells treated with unedited T cells are shown with open squares. The graph shows the mean ± SD from 3 technical replicates with increasing ratios of CTX130 or unedited T cells to tumor cells (0.125:1 to 4:1). D, Antitumor activity of CAR T cells in an RCC xenograft model. Mice were either left untreated ( n = 5) or injected with CTX130 ( n = 5) or CD70 + anti-CD70 CAR T cells ( n = 4). Each point represents the mean tumor volume ± SEM. E, Disruption of the PD-1 checkpoint gene is detrimental to CTX130 CAR T-cell function in a xenograft rechallenge model. Following the first injection of tumor cells, mice ( n = 5 per group) were left untreated (open circles) or treated with CTX130 (open squares) or PD1 − CTX130 CAR T cells (open triangles). At the day 25 rechallenge, fresh tumor cells were injected into the left flank of treated mice (CTX130-treated and PD1 − CTX130-treated animals represented by solid circles and solid triangles, respectively) and a new control group (open lozenges). Each point represents the mean tumor volume ± SEM. F, Mortality due to GvHD in mice ( n = 30 per group) treated with unedited T cells or low (20 million cells/mouse) or high (40 million cells/mouse) doses of CTX130. CAR, chimeric antigen receptor; CD, cluster of differentiation; EP, electroporation; GvHD, graft versus host disease; KO, knockout; PD-1, programmed cell death 1; RCC, renal cell carcinoma.

Article Snippet: The A498 adherent cancer cell line was trypsinized and seeded in ATCC-recommended media (EMEM + 10% FBS) in a 6-well plate (Corning Inc.; catalog no. 3506).

Techniques: Activity Assay, Lysis, Injection, Disruption, Cell Function Assay, Control, Electroporation, Knock-Out