In two preclinical breast cancer xenograft models (abstract #431P), PIKTOR inhibited tumor growth to a comparable or greater extent than intravenous gedatolisib PIKTOR inhibited HR+/HER2- breast cancer xenograft tumor growth in models with and without a PIK3CA mutation, the same population FTH-PIK-101 enrolls In mouse xenograft models, PIKTOR in combination with fulvestrant and palbociclib achieved complete tumor growth inhibition or tumor regression. This combination is being tested in FTH-PIK-101 In a kinase assay, PIKTOR inhibited AKT more deeply than single-node PAM inhibitors at clinically relevant concentrations These data lend support for Faeth’s multi-node strategy, with two upcoming readouts: FTH-PIK-201 topline data in second-line advanced endometrial cancer by year-end 2026 and FTH-PIK-101 interim data in HR+/HER2- advanced breast cancer in 2027 AUSTIN, Texas --(BUSINESS WIRE)-- Faeth Therapeutics (Nasdaq: FTH), a clinical-stage oncology company developing multi-node therapies for cancer patients, including its lead program PIKTOR, today announced presentation of preclinical data at the European Society for Medical Oncology (ESMO) Congress 2026 in Madrid, Spain , in a poster entitled “Characterising the efficacy of multi-node PI3K/AKT/mTOR pathway inhibition with serabelisib and sapanisertib (PIKTOR) in combination with SERDs and a CDK4/6 inhibitor in models of HR+/HER2- breast cancer.” These data support the design of FTH-PIK-101, the ongoing Phase 1b/2 clinical trial of PIKTOR with fulvestrant and/or other anticancer therapies in HR+/HER2- advanced breast cancer. In xenograft models with and without a PIK3CA mutation, oral PIKTOR inhibited tumor growth to a comparable or greater extent than intravenous gedatolisib. In combination with fulvestrant and palbociclib, standard-of-care treatments for HR+/HER2- breast cancer, PIKTOR completely inhibited tumor growth. In a cell-derived assay, PIKTOR achieved a greater degree of AKT kinase inhibition compared to single-node inhibitors, including other alpha-selective PI3K and/or mTOR inhibitors. Faeth believes these findings support the potential for an all-oral, multi-node option to improve on the standard of care in breast cancer, and expects FTH-PIK-201 topline data in second-line advanced endometrial cancer by year-end 2026 and FTH-PIK-101 interim data in 2027. “These data strengthen our conviction that oral multi-node inhibition of the PI3K/AKT/mTOR pathway is achievable and that PIKTOR can work alongside standard of care,” said Anand Parikh , Chief Executive Officer of Faeth Therapeutics . “In HR+/HER2- advanced breast cancer, we believe PIKTOR may offer patients an all-oral option designed to address the limits of single-node inhibitors, and it could give Faeth a differentiated position relative to gedatolisib, another multi-node inhibitor which is intravenous by design. We believe we can translate this science into clinical evidence, with topline data from our Phase 2 FTH-PIK-201 trial in second-line advanced endometrial cancer by year-end 2026 and interim data from our Phase 1b/2 FTH-PIK-101 trial in breast cancer in 2027.” Data summary Xenograft studies in mice with human breast cancer tumors Design: Faeth ran four studies in mice implanted with human HR+/HER2- breast cancer cells: two with MCF7 cells, which carry a PIK3CA mutation, and two with HCC1428 cells, which do not. After tumors formed, mice received PIKTOR, gedatolisib, palbociclib, fulvestrant, or combinations of these. PIKTOR alone: PIKTOR slowed tumor growth compared with no treatment in both tumor types. PIKTOR versus gedatolisib: In the MCF7 model, tumor growth inhibition was comparable. In the HCC1428 model, PIKTOR achieved greater tumor growth inhibition than gedatolisib with or without the combination of fulvestrant and palbociclib. Combinations: PIKTOR enhanced the activity of fulvestrant and palbociclib. The triple combination halted tumor growth in the HCC1428 model and shrank tumors in the MCF7 model. Pathway assays AKT activity: In cell lysates, PIKTOR reduced AKT activity to ~10% of uninhibited levels, a deeper reduction than any of the other PI3K and/or mTOR inhibitors tested. AKT is a central signaling node downstream of PI3K along the PAM axis that tumors rely on for growth and survival. Phosphorylation assay: In both breast cancer cell lines, Faeth measured PIKTOR’s ability to alter phosphorylation levels of key PAM nodes (PI3K, AKT, and mTOR). Phosphorylation status is another measure of pathway activity. PIKTOR suppressed phospho-AKT, phospho-S6, and phospho-4E-BP1, consistent with its design to block the PI3K/AKT/mTOR pathway at more than one point. The poster is available on the Publications tab of the Faeth website at https://www.faeththerapeutics.com/science#publications . Presentation Details: Title: Characterising the efficacy of multi-node PI3K/AKT/mTOR pathway inhibition with serabelisib and sapanisertib (PIKTOR) in combination with SERDs and CDK inhibitors