We know from experience that innovation doesn’t follow the beaten path, and that fresh ways of thinking can be the only way to shift existing paradigms. Our modular engineering approach is uniquely positioned to revolutionize T cell therapies.
Multiple binders that target multiple tumor antigens. Co-stimulatory signaling domains that can be tuned to endow CAR* T cells with optimal functionality and persistence. Armors, switches, and enhancers that further optimize CAR T functionality and overcome the immunoinhibitory environment of cancers.
*CAR = chimeric antigen receptor.
Microenvironment modulation to counter the immunosuppressive tumor environment. Altered cytokine profiles that modulate toxicity and efficacy. Allogeneic CAR* T cells may be developed based on successful autologous products.
*CAR = chimeric antigen receptor.
Vector and cell manufacturing with Penn and Strategic Collaborators for rapid clinical development.
Tmunity’s proprietary binders recognize a range of targets on solid tumors. Multiple binders can be deployed within a cell to deal with variable tumor antigen expression.
| B-cell binders | B-cell malignancies |
| Plasma cell binders | Plasma cell malignancies |
| PSMA, PSCA | Prostate cancer |
| TnMUC1 | Pancreatic, Non–Small Cell Lung, Triple-Negative Breast, Ovarian |
| EGFR | Glioblastoma |
| IL13Rα2 | Glioblastoma, Pancreatic |
| GPC2 | Neuroblastoma, Small Cell Lung, Neuroendocrine Tumors |
| Mesothelin | Lung, Ovarian, Pancreatic, Mesothelioma |
| FAP | Prostate, Lung, Pancreatic, Breast, Ovarian, Oral, Gastric, Colon, Glioblastoma, Esophageal, Mesothelioma |
Antigen Recognition
Modules dial up or down the “engine” of T cell activation, with the potential to create CAR Ts with the optimal profile for efficacy, safety, and persistence needed to eradicate a variety of solid tumors.
| CD2 |
| 4-1BB |
| ICOS |
| CD27 |
Co-stimulatory Domains
Modular vectors endow T cells with a suite of capabilities that potentially balance efficacy and safety, optimizing T cells for specific solid tumor targets:
| dnTGF-βRII |
| TGF-β/IL-12R |
| PD-1/CD28 switch receptor |
| IL-18 secretion |
Armors, ENHANCERS, Switches
To counter the immunosuppressive tumor environment, T cells can be highly engineered to block the effects of cytokines/checkpoints and translate negative immuno-inhibitory signals into positive signals for cell activation and function.
| dnTGF-βRII:
Improves CAR T proliferation and expansion potential by neutralizing TGF-β signaling. |
| TGFβ/IL-12R:
Improves CAR T potency by switching the inhibitory effects of TGF-β signaling into a stimulatory IL-12R signal. |
| PD-1/CD28 switch receptor:
Improves CAR T antitumor activity and reduces tumor-induced inhibition by leveraging the overexpression of PD-L1 on tumor cells and switching its inhibitory effects into a stimulatory CD28 signal. |
T cell engineering can increase or decrease the presence of important cytokines and modulate their effect in the tumor microenvironment.
| CRISPR editing of GM-CSF may result in reduced toxicity and enhanced antitumor activity. |
| IL-18 secretion may enhance CAR T cell expansion and increase effectiveness of antitumor activity. |
As a next step in our cell engineering platform evolution, we intend to adapt the gene editing and vector delivery capabilities proven in the autologous setting to develop allogeneic CAR T therapies.
Gene Editing
We have the ability to knock out genes of interest by using technologies
like CRISPR multiplex genome editing.
Vector Systems
We believe our vector systems will be able to deliver next generation
CARs into gene-edited allogeneic T cells.
Our allogeneic CAR T therapies will aim to achieve the following:
