Company: LIMN
Filing Date: 2025-07-28
Form Type: S-1/A
Source: 0001410578-25-001518
Chunk: 139

Company: Liminatus Pharma, Inc.
Filing Date: 2025-07-28
Form: S-1/A
Chunk 139
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 has the potential to become a significant treatment option for cancer patients. Checkpoint Inhibitor CD47 A critical feature of the immune system is its ability to distinguish between normal cells in the body and those deemed as “foreign” (such as germs and cancer cells). This allows the immune system to attack the foreign cells while leaving normal cells unharmed. The immune system does this, in part, by using “checkpoint” proteins on immune cells. The checkpoints act like switches that need to be turned on or off to start an immune response. But tumors can find ways to manipulate these on/off immune checkpoints to avoid being attacked by the immune system. Monoclonal antibodies targeting immune checkpoints are designed as therapies to forcefully activate the “on” switch of the immune response, allowing the immune system to mount an effective anti-tumor attack. These medicines, known as immune checkpoint inhibitors, work by targeting checkpoint proteins to block the tumor’s ability to shut down the immune response and thereby induce a potent anti-cancer effect. Rather than killing cancer cells directly, they aid the immune system to detect and mount an attack on cancer cells. Several therapeutics that target different checkpoint proteins have been approved to treat some types of cancer including PD-1 (Pembrolizumab, Merck & Co; Novolumab, BMS; Cemiplimab, Regeneron), PD-L1(Atezolizumab, Genentech; Avelumab EMD Serono & Pfizer; Durvalumab, AstraZeneca), CTLA-4 (Ipilumab, BMS; tremelimumab, AstraZeneca), and LAG-3 (Opdulag, BMS) inhibitors. Although such therapies have revolutionized cancer treatment showing to be remarkably effective in certain subsets of patients with specific types of tumors, there are a significant number of cancer patients for whom these therapies are not effective. Another novel, yet well-established immune checkpoint is CD47 which plays a broad role in cancer immune evasion across multiple cancers. CD47 is a transmembrane protein, an integral membrane protein that spans the entirety of the cell membrane, and upon its interaction with SIRPα, which is expressed on macrophages, a “don’t eat me” signal is sent to the macrophages. This helps tumors achieve immune escape by stopping macrophages from acting on these tumor cells to undergo phagocytosis. Blockade of the interaction between CD47 and SIRPα could