Immunotherapy alone has a response rate of roughly 8% to 13% in ovarian cancer when all subtypes are grouped together. That’s lower than in many other cancers, which is why ovarian cancer has historically been considered a tough target for immune-based treatments. But those numbers shift significantly depending on the type of ovarian cancer, specific tumor characteristics, and whether immunotherapy is paired with other drugs.
Why Overall Response Rates Are Low
Ovarian cancer, particularly the most common form (high-grade serous), tends to create an environment that suppresses immune activity. The tumors often have fewer genetic mutations than cancers where immunotherapy works well, like melanoma or lung cancer. Fewer mutations generally means fewer signals for the immune system to recognize and attack. Studies of single-agent checkpoint inhibitors across all ovarian cancer subtypes have consistently shown objective response rates between 8% and 13%, meaning that roughly one in ten patients sees measurable tumor shrinkage.
Tumor Markers That Predict Better Results
Two biomarkers can identify patients more likely to benefit: PD-L1 expression and a DNA repair defect called microsatellite instability-high (MSI-H).
PD-L1 is a protein that tumors use to hide from the immune system. Checkpoint inhibitors block this protein, making the tumor visible again. In the KEYNOTE-100 trial of pembrolizumab, patients whose tumors had higher PD-L1 scores (measured by a system called the Combined Positive Score, or CPS) responded more often. Those with a CPS of 10 or above had a 17.1% response rate, compared with less than 15% for lower scores. That’s an improvement, but it still means the majority of patients in the highest-scoring group didn’t respond. PD-L1 testing helps narrow the field, though it isn’t a perfect predictor. Some patients with high scores don’t respond, and some with low scores do.
MSI-H tumors have a defect in their ability to repair DNA, which causes them to accumulate many more mutations than usual. That abundance of mutations makes them far more visible to the immune system. In the large KEYNOTE-158 trial, which studied pembrolizumab across many MSI-H cancer types, the overall response rate was 30.8%, and responses were remarkably durable, lasting a median of nearly four years (47.5 months). The catch is that MSI-H tumors are rare in ovarian cancer, occurring in only a small percentage of cases.
Clear Cell Ovarian Cancer Responds Differently
Not all ovarian cancers behave the same way. Clear cell carcinoma, which accounts for roughly 5% to 10% of ovarian cancers, appears more responsive to immunotherapy than the dominant high-grade serous type. In one phase 2 trial, the combination of pembrolizumab with an immune-modulating drug called epacadostat produced a 21% response rate in patients with recurrent clear cell ovarian cancer. A separate randomized study found that patients with clear cell tumors were five times more likely to respond to immunotherapy than patients with other subtypes.
This matters because clear cell ovarian cancer is notoriously resistant to standard platinum-based chemotherapy, with response rates below 10% for recurrent disease. Immunotherapy may offer a comparatively better option for this specific group, even though the absolute numbers remain modest.
Combination Approaches and the First FDA Approval
Pairing immunotherapy with other treatments has been the major strategy to push response rates higher. In 2025, the FDA approved the first immunotherapy specifically for ovarian cancer: pembrolizumab combined with weekly paclitaxel (a chemotherapy drug), with or without bevacizumab (a drug that starves tumors of their blood supply). This approval covers a specific group of patients: those with platinum-resistant disease whose tumors test positive for PD-L1 and who have received one or two prior treatments.
This approval marks a significant shift. For years, immunotherapy was available to ovarian cancer patients only through clinical trials or through tumor-agnostic approvals (like the MSI-H indication). Having a dedicated approval means more patients with platinum-resistant disease now have an additional treatment option backed by regulatory review of safety and efficacy data.
Other combinations are also being studied. A trial of pembrolizumab combined with lenvatinib, a drug that targets blood vessel growth and certain signaling pathways, showed a median progression-free survival of 6.2 months and an overall survival of 21.3 months in previously treated patients. While these numbers reflect incremental progress rather than dramatic breakthroughs, they suggest that multi-drug strategies can extend the window of disease control.
What “Success” Looks Like in Practice
When immunotherapy does work in ovarian cancer, it can work for a long time. The durability of response is one of its most notable features. In the KEYNOTE-158 trial of MSI-H cancers, the median duration of response was 47.5 months. That’s nearly four years of sustained tumor control, far longer than what chemotherapy typically achieves. Even in broader ovarian cancer populations, some patients who respond to immunotherapy maintain that response for years, a phenomenon sometimes called a “tail on the curve” because these long-term responders create a distinctive pattern on survival graphs.
The challenge is that most ovarian cancer patients don’t fall into that fortunate group. The overall picture is one of low probability but high reward: a relatively small percentage of patients respond, but those who do often experience meaningful, lasting benefit. This is why biomarker testing (PD-L1, MSI-H) matters so much. It helps identify the patients most likely to be in that responsive group, sparing others from treatment that is unlikely to help them and may cause immune-related side effects like fatigue, skin reactions, thyroid problems, or inflammation in various organs.
How Ovarian Cancer Compares to Other Cancers
For context, single-agent checkpoint inhibitors achieve response rates above 40% in melanoma and around 20% to 25% in non-small cell lung cancer. Ovarian cancer’s 8% to 13% rate places it toward the lower end of the spectrum, alongside cancers like prostate and pancreatic cancer that are also considered “immunologically cold.” The MSI-H subgroup is the exception, performing comparably to more responsive cancer types, but it represents a small fraction of ovarian cancer diagnoses.
The gap between ovarian cancer and more responsive tumor types has driven ongoing research into why the ovarian tumor environment is so effective at suppressing immune responses and how that suppression might be overcome through new drug combinations or treatment sequences.