The drug exhibits a multimodal mechanism. It not only reverses chemoresistance and halts tumor growth but also 'turns cold tumors hot' by forcing cancer cells to display markers that make them visible to the immune system. This dual action of direct attack and immune activation creates a powerful synergistic effect.

Step Pharma's synthetic lethality approach targets two redundant enzymes in the same pathway. Deleting one makes cancer cells entirely dependent on the other. This direct dependency is harder for biology to circumvent compared to approaches targeting different, interconnected pathways, creating a "cleaner" kill mechanism.

Many peptides are unlikely to ever receive FDA approval because their simple, easily replicated structures make them commodities. Pharma companies won't fund billion-dollar trials for drugs they can't patent, leaving them in a permanent gray market.

The degradation mechanism is fundamentally superior to inhibition because it removes the entire protein, addressing both its enzymatic and scaffolding functions. This allows degraders to hit targets harder and more completely, suggesting they could become the dominant modality across oncology and other therapeutic areas.

An innovative strategy for solid tumors involves using bispecific T-cell engagers to target the tumor stroma—the protective fibrotic tissue surrounding the tumor. This novel approach aims to first eliminate this physical barrier, making the cancer cells themselves more vulnerable to subsequent immune attack.

Accession's second product is a bispecific antibody that binds to all cancer cells. While this would be dangerously toxic if delivered systemically, their targeted virus delivery system ensures it is only produced inside the tumor. This strategy makes previously "undruggable" therapeutic concepts viable.

Counterintuitively, administering super-physiologic levels of testosterone can induce responses in certain castration-resistant prostate cancers. This strategy, called Bipolar Androgen Therapy, exploits the tumor's overexpressed receptors, turning a growth signal into a therapeutic vulnerability, though it remains a risky approach.

Instead of just killing cancer cells, the primary mechanism is to insert a gene that forces the infected cell to produce and secrete a potent drug, like an anti-PD-L1 antibody. This creates a hyper-concentrated therapeutic effect directly in the tumor microenvironment, a concept termed "molecular surgery."

Unlike VEGF TKIs that primarily target the tumor vasculature, the HIF-2 inhibitor belzutifan has a direct anti-tumor cell effect. This mechanism may be uniquely effective against micrometastatic disease, following the logic of traditional chemotherapy. This distinction could explain its surprising success in the adjuvant setting where multiple VEGF TKIs have failed.