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.

To overcome on-target, off-tumor toxicity, LabGenius designs antibodies that act like biological computers. These molecules "sample" the density of target receptors on a cell's surface and are engineered to activate and kill only when a specific threshold is met, distinguishing high-expression cancer cells from low-expression healthy cells.

Pathways like integrins have long been of interest but lacked effective therapeutic approaches. The advent of new technologies, such as antibody-drug conjugates and checkpoint inhibitors, has created opportunities to re-explore these older targets with potent, modern drugs, breathing new life into decades-old research.

The efficacy of some established drugs, like the chemotherapy oxaliplatin, may be due to an unknown mechanism: they partition into and disrupt cellular condensates. This reframes our understanding of drug action and could explain why certain drugs are more effective in some cancers than others.

Cancer should be viewed not just as rogue cells, but as a complex system with its own supply chains and communication infrastructure. This perspective shift justifies novel therapies like Zelenorstat, which aim to dismantle this entire operating system by cutting its power source.

Traditional targeted cancer therapies inhibit or 'cool down' overactive pathways, like pumping brakes on a runaway car. Delpha Therapeutics employs a counterintuitive 'activation lethality' approach, further over-activating pathways to 'overheat the engine' and cause catastrophic failure in cancer cells—a fundamentally opposite but highly effective strategy.

The same cellular mechanism (NMT) hijacked by cancer cells is also exploited by viruses like HIV and coronaviruses for replication. By inhibiting NMT, Zelenorstat could potentially halt viral spread, making it a candidate for future pandemic defense.

Instead of searching for elusive natural markers to target, EARLI's platform creates its own. It programs synthetic genetic "switches" that activate only inside cancer cells, turning them into factories that produce their own cancer-fighting therapies. This shifts the paradigm from biological discovery to biological engineering.