Kairos Pharma, Ltd. LD Micro 20th Annual Main Event Conference

Thank you. Thank you for joining us this afternoon. Here are forward-looking statements, too small to read. Our mission at Kairos Pharma is to advance therapies that overcome critical challenges in cancer drug resistance and immune suppression. The problem is that resistance develops to even blockbuster drugs like antiandrogen therapies in prostate cancer and Tagrisso in non-small cell lung cancer. The solution is that CD105 is elevated as the cancer cells become resistant, and our antibody, ENV-105, reverses this resistance. These are large opportunities in prostate cancer, non-small cell lung cancer, and other tumor types. We have three clinical programs in progress. Our lead drug, ENV-105, in phase II trial, is treating prostate cancer with NIH grant funding. ENV-105 is also in a phase I trial treating non-small cell lung cancer with non-dilutive donor funding.

We have an experienced team at Cedars-Sinai to drive enrollment and grant funding to create non-dilutive value. Our prostate trial is a phase II trial that is randomized between 80 patients. Our lung cancer trial is a 60-patient trial, and the glioblastoma trial is getting underway and funded by a donor. We have solid tumors that will be treated with KROS-101 with grant funding. Resistance develops to many different types of therapies, including tyrosine kinase inhibitors like Tagrisso, radiation therapy, immune therapy, and hormone therapy. In our prostate trial and lung trial, tumors become resistant, and this is through a mechanism of CD105 which becomes elevated during treatment. What CD105 does is it targets a molecule called BMP4. BMP4 is involved in making a cancer more stem cell-like.

What that means is in parallel to normal stem cells in the organs that drive all of the cells of a particular organ, cancer stem cells drive the cancer cells to become more stem cell-like. What that means is the stem cells are important cells that make all of the cells of the organ. It differentiates to all of the cells. In a similar fashion, cancer stem cells drive and initiate the cancer and make all of the tumor cells of that cancer. What CD105 does is by signaling BMP4, cells become more stem cell-like, and stem cells are known to be resistant to different types of toxins in the environment.

Just like normal cells need to be resistant to radiation and to the toxins in the environment to be able to recreate all the cells of the organ, cancer stem cells are resistant to radiation and the therapeutics that are used to treat it. As BMP4 signaling is made by CD105, the cancer cells become more cancer stem cell-like and resistant to the drugs. Here you can see when you look at lung cancer patients, the expression of CD105 is directly related to their overall survival. Here you see the survival of patients with a high CD105 expression and a low CD105 expression. Survival is significantly longer in the low CD105-expressing patients. There are 45,000 patients with EGFR-driven non-small cell lung cancer, and Tagrisso is the standard of care for these patients.

We demonstrated in an animal model that when you compare a treatment with Tagrisso or osimertinib, there is a significant decrease in the growth of these tumors when you add ENV-105, otherwise known as carotuximab. Based on these data and other data, we went into a phase I trial with Tagrisso to see if our drug would make these patients go longer on Tagrisso. This is our phase I trial with 20 patients on Tagrisso that are resistant and 20 patients that are incompletely treated with Tagrisso, which we are actively accruing on. We recently reported the safety results. There were no grade 3 or higher toxicities in 11 patients treated to date on ENV-105. An interim efficacy readout will be reported this quarter in 2026. ENV-105 restores sensitivity to hormone therapy in this human tumor.