Pamela Holland, PhD, is SVP of Biology at InduPro, overseeing pipeline development.
Prior to InduPro, she was SVP of Research at Alpine Immune Sciences, overseeing oncology and autoimmunity programs. Prior to Alpine, she was VP, Cancer Biology at Surface Oncology in Cambridge MA, playing key roles in developing the early Surface pipeline and establishing a multi-program strategic partnership with Novartis. Prior to Surface, Dr. Holland held roles of increasing responsibility in oncology research at Amgen, working on TNF-receptor superfamily members for oncology and cancer immunotherapy. Dr. Holland obtained her PhD from the University of Washington/Fred
Hutchinson Cancer Research Center followed by a post-doctoral position at Immunex.
Prior to graduate school, she was a key contributor to the development of PCR applications and TaqMan™at Cetus Corporation. She is a co-inventor on all TaqMan patents and was the lead author on the first publication describing TaqMan in 1991.

InduPro is developing novel therapeutics by leveraging protein proximity at the cell surface.  We have observed that re-localization of immunomodulatory proteins into or out of an immune synapse by engineering select bi-specific antibodies can dramatically influence T cell activity.  We looked for proteins inherently proximal to PD-1 using our proprietary cell surface proximity labeling platform.  Here, we describe IDP-003, a differentiated PD-1 agonist bispecific antibody that recruits PD-1 to the synapse by bridging it in cis to the co-stimulatory receptor CD2. Expression of CD2 ligand CD58 on APCs, but not T cells, is required for IDP-003 activity, which promotes PD-1 phosphorylation and potent T cell suppression. Importantly, IDP-003 is not dependent on FcR engagement for activity and is devoid of limitations associated with FcR polymorphisms that alter Fc-FcR binding affinities.  IDP-003 promotes agonistic signaling through PD-1 and is expected to have activity in multiple indications where pathogenic PD-1+ T cells are drivers of autoimmune disease. Examples of sequestration of PD-1 away from the immune synapse by developing novel PD-1 bispecific antagonists will also be presented.  By manipulating the immune synapse, we have devised new therapeutic targeting strategies for PD-1 agonism and antagonism.

• Localization of immunomodulatory proteins into or out of the immune synapse using bispecific antibodies can alter T cell activation states
• IDP-003 is a differentiated PD-1xCD2 bispecific antibody that localizes PD-1 to the synapse by bridging it in cis to the co-stimulatory receptor CD2 and functions as a PD1 agonist
• IDP-003 promotes PD-1 phosphorylation and potent T cell suppression independently from FcR engagement and may have clinical application in multiple autoimmune disorders