Figure 1.
PRMT5 inhibition via PRT382 is effective at killing MCL in vitro and in vivo. (A) IC50 of 9 MCL cell lines measured by annexin V/PI staining and flow cytometry on day 9. (B) Survival of CCMCL1-engrafted NSG mice treated with PRT382 at varying doses and frequencies. PRT382 10 mg/kg 4D3D showed the greatest survival advantage (P < .01). QD – daily, 4D3D – 4 days on treatment, 3 days off QOD – every other day. (C) Circulating huCD19+ cells in CCMCL1-engrafted NSG mice. PRT382 treatment significantly delayed disease progression. A log-rank test with significance was used for panel B. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. Error bars show standard deviation of the data.

PRMT5 inhibition via PRT382 is effective at killing MCL in vitro and in vivo. (A) IC50 of 9 MCL cell lines measured by annexin V/PI staining and flow cytometry on day 9. (B) Survival of CCMCL1-engrafted NSG mice treated with PRT382 at varying doses and frequencies. PRT382 10 mg/kg 4D3D showed the greatest survival advantage (P < .01). QD – daily, 4D3D – 4 days on treatment, 3 days off QOD – every other day. (C) Circulating huCD19+ cells in CCMCL1-engrafted NSG mice. PRT382 treatment significantly delayed disease progression. A log-rank test with significance was used for panel B. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. Error bars show standard deviation of the data.

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