Anyone think desmoplasia (growth of fibrous or connective tissue) could be a target for LL? I ask as I learn more terms related to pancreatic ductal adenocarcinoma because a close friend was diagnosed in later stages. He’s about 2-3 months into baseline treatment of abraxane/gemcitabine, which apparently has a near 100% failure rate within 12 months. Some version of immunotherapy may be chosen next but it’s apparently not part of current 1st level SOC.

So. From what I understand, chemoresistance rises with desmoplasia, and pancreatic stellate cells (PaSC) are key drivers of that fibrosis. I’ve seen the list of cytokine signals that LL regulates. And some of activating factors for PaSC are on the ohm list, the latest of which starts with MapK and goes to TGF-b.

The friend is a physician and naturally is following current treating protocol. I’m not a clinician, so it’s a short conversation about MABs with a clinician not inclined to seek a safe treatment even if efficacy for a specific indication is not yet fully realized. Thus I pass to him all I unearth in papers, citations about LL/MABs so he can have that peer chat.

Any strategy would be most appreciated for prompting someone to fully vet LL when considering it on a right-to-try basis for a broad scope need in pancreatic cancer. Many thanks.