Tridek-One develops first-in-class anti-CD31 agonistic antibodies to restore immune balance in patients with autoimmune and inflammatory diseases. By targeting the CD31 pathway, these compounds aim to modulate leukocyte activation and reduce tissue damage associated with excessive immune responses.
Funding
$20.1M raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Founders
Product
Problem
Autoimmune and inflammatory diseases result from an imbalance in the immune system, leading to excessive immune responses and tissue damage. Current treatments often lack specificity and can result in broad immunosuppression, increasing the risk of infection and other complications.
Solution
Tridek-One Therapeutics is developing first-in-class bispecific antibodies that act as CD31 checkpoint agonists to restore immune balance in patients with autoimmune and inflammatory diseases. Their therapeutic approach involves targeting CD31, an inhibitory receptor expressed on various immune cells, in combination with cell-specific ITAM receptors. This dual-targeting strategy enables selective immunomodulation of pathogenic immune cells, reducing the risk of systemic immunosuppression. By engaging CD31, these antibodies activate intracellular signaling pathways that inhibit leukocyte activation, proliferation, and cytokine production, thereby dampening excessive immune responses and preventing further tissue damage.
Target Audience
The primary target audience includes pharmaceutical companies, clinical investigators, and ultimately patients with autoimmune and inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel disease.
Features
- First-in-class anti-CD31 agonistic bispecific antibodies for targeted immunomodulation.
- Dual-targeting approach combining anti-CD31 and ITAM-targeting moieties for cell-specific action.
- IgG-like pharmacokinetic (PK) properties for optimized drug delivery and efficacy.
- Selective targeting of pathogenic immune cells to minimize systemic immunosuppression.
- Modulation of neutrophil activation and recruitment to promote resolution of inflammation.
- Inhibition of T cell activation by blocking TCR signaling pathways.
- Suppression of B cell signaling by interfering with BCR activation.