Memo Therapeutics CEO Erik van den Berg explains the BK virus, dormant in 90% of the population, reactivates under severe immunosuppression required for organ transplants. This doubles the risk of kidney graft failure and triples the risk of death for these patients, who currently have no available treatment.
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To overcome the industry bottleneck of few validated solid tumor targets (15-20), Memo analyzes tumor-infiltrating B-cells from patients with superior outcomes. This approach aims to identify unique antibody-target pairs, unlocking new biological pathways for next-generation therapies like ADCs and CAR-Ts.
To overcome the historical issue of oncolytic viruses being sequestered by the liver, Accession re-engineers a human virus so it cannot infect any human cells. Only after this safety step is it re-targeted to infect only cancer cells, ensuring precise delivery and avoiding systemic side effects.
Early-stage biotech companies struggle to navigate clinical development for autoimmune diseases. Disease-specific foundations hold crucial insights on patient subsets, recruitment, and key opinion leaders, yet the interface between VCs and these foundations is often inefficient and difficult to navigate, leading to missed opportunities and flawed trial execution.
Frustration with traditional antibody discovery, which captures only 1% of a sample's B-cell diversity, led to Memo's microfluidics platform. CEO Erik van den Berg states their technology retains over 80% of the B-cell information, enabling the discovery of rare, super-potent human antibodies that would otherwise be lost.
The primary hurdle for the entire biologics field is enhancing the therapeutic index (efficacy vs. toxicity). Because most conditions like cancer and autoimmune disorders are 'diseases of self,' therapeutics often have on-target, off-tumor effects. This fundamental problem drives the need for innovations like masking and conditional activation.
Erik van den Berg highlights a critical paradox in the current standard of care for BK virus infections post-transplant. The only available intervention is lowering immunosuppression to fight the virus, but this simultaneously increases the probability that the patient's immune system will reject the newly transplanted organ.
A key innovation in Sana's diabetes cell therapy is overcoming the dual immune response. While knocking out MHC expression hides cells from the adaptive system (T-cells), this triggers an attack from the innate system (NK cells). Sana's solution is to overexpress CD47, effectively creating a "don't kill me" signal for both.
Modern critical care for sepsis only treats the consequences of the disease—organ failure, low blood pressure—with supportive measures like ventilators and IV fluids. There are zero approved therapies that actually treat the underlying root cause: the out-of-control immune response that is actively damaging the patient's body.
A sophisticated concern regarding the HIF-2 inhibitor belzutifan is its potential to diminish kidney cancer's antigenicity by reducing human endogenous retrovirus expression. While providing an early benefit, this could theoretically make tumors less responsive to subsequent immunotherapies, negatively impacting long-term outcomes—a critical consideration for sequencing.
Dr. Radvanyi explains that immune agonist drugs often fail because accelerating a biological pathway is inherently less controllable than inhibiting one. This is analogous to genetic knockouts being more straightforward than over-expression models, presenting a core challenge in drug development beyond just finding the right target.
