AT-1965

AT-1965 (88 mg/kg; i.v.; days 9 and 10 (cycle 1), days 15 and 16 (cycle 2)) induces complete tumour regression and durable immune memory, as tumour-regressed mice show no tumour growth upon 4T1 rechallenge^[1].
AT-1965 (88 mg/kg; i.v.; days 1, 2, 7 and 8)-mediated tumour inhibition is independent of CD4⁺ and CD8⁺ T cell activity, as efficacy is maintained even with T cell depletion^[1].
AT-1965 (88 mg/kg; i.v.; days 18, 19, 22 and 23)-mediated anti-tumour efficacy is dependent on functional B cells, as efficacy is abrogated in B cell-deficient mice despite intact innate immune cells and T cells^[1].
Adoptive transfer of B cells from AT-1965 (88 mg/kg; i.v.; days 1, 2, 6 and 7 (donor mice))-treated tumour-regressed mice confers anti-tumour protection in naive recipient mice, confirming B cells mediate AT-1965's anti-tumour activity^[1].
AT-1965 (88 mg/kg; i.v.; unspecified schedule matching prior 4T1 studies)-mediated anti-tumour efficacy is dependent on IFIT1 expression in cancer cells^[1].
AT-1965 (88 mg/kg; i.v.; days 1 and 2) induces an innate antiviral immune response in 4T1 tumours, characterized by increased type I interferon and IFIT1 expression, and transient formation of IFIT1-RNA complexes in plasma^[1].
AT-1965 (88 mg/kg; i.v.; days 1 and 2) treatment induces early increases in intratumoural IgM levels, and IgM from treated mice preferentially binds to AT-1965-exposed cancer cells^[1].
AT-1965 (88 mg/kg; i.v.; unspecified schedule matching prior tumour studies) synergizes with PD-1 inhibitors to enhance anti-tumour efficacy in LLC tumours, doubling the complete response rate compared to monotherapy^[1].