

Faeth Therapeutics just posted an 80% response rate in endometrial cancer by starving tumors of their metabolic fuel. Their secret weapon? A drug combo that shuts down the PI3K pathway at three points, paired with a prescribed diet that cuts off the supply lines.
Cancer cells are gluttons. They gobble up glucose, hoard nutrients, and hijack your body's metabolic machinery to fuel their growth. For decades, oncology has fought back with three main weapons: cut it out, poison it with chemo, or unleash the immune system. But what if you could just... stop feeding it?
That's the bet Faeth Therapeutics is making. And their early clinical data suggest it might actually be working.
The San Francisco-based company just reported Phase 1b results for Piktor, a combination therapy designed to shut down a tumor's metabolic engine at multiple points simultaneously. In patients with endometrial cancer, Piktor delivered an 80% response rate. To put that in context, chemo alone in similar patients typically keeps tumors at bay for about three to four months. Piktor patients? Roughly 11 months of progression-free survival.
Those are the kind of numbers that make oncologists sit up in their chairs.
To understand why Piktor matters, you need to know about one of cancer's favorite pathways: PI3K/AKT/mTOR. Think of it as the cell's internal Amazon delivery service. It controls how cells take in glucose, build new proteins, manufacture fats, and decide whether to grow or stay quiet. When this pathway gets mutated (which happens a lot in cancer), the delivery trucks never stop running.
Drug companies have been trying to block this pathway for years. The problem? It's like playing whack-a-mole. Block one part, and the pathway reroutes around the obstacle. Single-target PI3K inhibitors often triggered feedback loops that reactivated the very growth signals they were supposed to stop. Toxicity was ugly, too: rashes, blood sugar spikes, mouth sores.
Faeth's answer: don't hit one mole. Hit three at the same time.
Piktor combines two oral drugs with a chemotherapy backbone:

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By targeting PI3K at the top and mTOR at the bottom, Piktor aims for a full pathway shutdown instead of a partial one. It's the difference between turning off a faucet and cutting the water main.
Across 15 evaluable patients with various advanced solid tumors in Phase 1b, the overall response rate hit 47%. Among patients whose tumors carried mutations in the PI3K/AKT/mTOR pathway, that number jumped to 71%. Three patients had complete responses, meaning no detectable tumor remained.
But the endometrial cancer results stole the show. Three others saw substantial tumor shrinkage.
This is where Faeth goes from "interesting biotech" to "genuinely different company." Beyond the drugs, they're layering on something almost unheard of in oncology trials: a precision, insulin-suppressing diet.
The logic is elegant. PI3K signaling is heavily driven by insulin and a related hormone called IGF-1. If you can lower a patient's insulin levels through diet, you're essentially cutting the fuel supply to the pathway that Piktor is already blocking with drugs. You're attacking the tumor's metabolism from two directions: the signals and the substrates.
Preclinical data published in the British Journal of Cancer showed that combining the drugs with an insulin-suppressing diet drove tumor regression in endometrial and breast cancer models. It's not a juice cleanse or a wellness fad; it's a controlled metabolic intervention designed to exploit a specific biological vulnerability.
The Gynecologic Oncology Group (GOG) Foundation, one of the most respected cooperative groups in women's cancer research, was convinced enough to launch a dedicated Phase 2 trial (GOG-3111) that formally tests the diet component alongside the drugs. That trial is enrolling roughly 40 patients, with full results expected in the third quarter of 2026.
Faeth isn't just developing a cancer drug. They're testing whether metabolism itself can become a therapeutic axis in oncology, a so-called "fifth pillar" alongside surgery, radiation, chemotherapy, and immunotherapy.
If that sounds ambitious, consider the landscape. Cancer treatment has been dominated by two revolutions over the past 20 years: targeted therapies (like kinase inhibitors) and immune checkpoint blockers (like Keytruda). Both have saved countless lives. Both also fail in a large number of patients. The field desperately needs new angles of attack.
Metabolic oncology is one of the most promising candidates. Beyond Faeth, companies are exploring glutamine addiction, lipid metabolism, ferroptosis (a form of iron-dependent cell death), and metabolic reprogramming of immune cells in the tumor microenvironment. AstraZeneca has a lactate transport inhibitor (AZD3965) in early trials. IDH inhibitors like ivosidenib and vorasidenib have already been approved for specific mutation-driven cancers.
But Faeth's approach is arguably the most holistic: drugs plus diet plus data science, all coordinated through their MetabOS platform, which uses machine learning to match tumor genotypes with specific metabolic vulnerabilities.
Let's be honest about the caveats, because there are real ones.
The Phase 1b data come from a small, non-randomized trial. Fifteen patients across all tumor types; ten in the endometrial cohort. Those response rates are eye-catching, but small numbers can be deceiving. The 11-month PFS is compared to a historical benchmark, not a head-to-head control arm.
Toxicity also deserves scrutiny. PI3K and mTOR inhibitors are notorious for causing hyperglycemia (high blood sugar), which is particularly tricky in endometrial cancer patients who often already have obesity and diabetes. The irony of prescribing an insulin-suppressing diet alongside drugs that can spike blood sugar is not lost on clinicians.
And the diet itself raises practical questions. Can patients actually follow a prescribed eating plan while undergoing cancer treatment? Will the GOG trial's dietary substudy prove the added benefit, or will adherence issues muddy the results?
The GOG Phase 2 readout, expected in Q3 2026, will be the real inflection point. If the response rates hold up in a larger, multi-center setting (and if the diet component shows measurable benefit), Faeth could validate an entirely new way of thinking about cancer treatment.
Sapanisertib combined with paclitaxel earned a late-breaking oral presentation at ESMO based on Phase 2 data from the DICE trial in ovarian cancer, one of the world's premier oncology conferences. That kind of spotlight is reserved for results the scientific community considers potentially practice-changing.
Faeth was acquired by Sensei Biotherapeutics (Nasdaq: SNSE) in early 2026, bringing roughly $200 million in new capital to push the program forward. The original investors, including Khosla Ventures and S2G Ventures, had put in about $92 million over several rounds since the company's founding in 2019.
The bottom line: Faeth is asking whether we've been so focused on killing cancer cells that we forgot to ask what they eat. The early answer is promising. The definitive one is a few months away.
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