Stock of Cue fell after posting negative early combo data of its IL-2 with Keytruda in HNC

CLINICAL AND REGULATORY

ImmunityBio announced promising study results that demonstrate the activation of CD4+ and CD8+ T cells and natural killer (NK) cells in people living with HIV by ImmunityBio’s IL-15 superagonist Anktiva (N-803). Anktiva stimulates latent HIV replication (the ‘kick’) in CD4 memory cells allowing the previously hidden infected cells to be revealed to and eliminated (the ‘kill’) by CD8 and NK cells. This mechanism is key for killing cells that harbor latent virus, thereby reducing viral reservoirs in anti-retroviral (ART)-suppressed HIV patients and ultimately ridding the body of the virus and the threat of re-activation. These positive clinical findings support ImmunityBio’s “Kick-and-Kill” strategy to cure HIV. In both pre-clinical and clinical research, ImmunityBio’s IL-15 superagonist Anktiva has exhibited three activities that could potentially help the immune system eliminate HIV reservoirs and control virus rebound. First, Anktiva has been shown to reverse HIV latency, whereby genetic code for the virus persists, but virus is not made, allowing the infected cells to evade detection and elimination by the immune system, by stimulating HIV replication within long-lived immune cells such as memory CD4 cells, allowing the infected cells to be recognized and cleared. Second, it activates NK cells and CD8+ T-cells, two elements of the immune system that specialize in killing virus-infected cells. Third, it enables NK cells and CD8+ T-cells to move to lymphoid tissues where they will encounter and have an increased likelihood of eliminating HIV-infected cells.

Cue Biopharma falls after early combination data in head and neck cancers

Cue fell 25% after announcing that two of four patients with recurrent or metastatic HPV+ head and neck cancers achieved a partial response to lead candidate CUE-101 plus Keytruda pembrolizumab. Patients were treated at the 2 mg/kg dose of CUE-101, which combines IL-2 with two tumor-antigen bound HLA molecules to stimulate endogenous antitumor T cells. One partial response was unconfirmed.