Platinum-resistant ovarian cancer remains one of the most difficult settings in gynecologic oncology. In the US, about 21,010 women are expected to receive a new diagnosis of ovarian cancer in 2026, and about 12,450 women are expected to die from the disease.
While many patients initially respond to platinum-based chemotherapy, advanced ovarian cancer frequently recurs, and many patients with recurrent disease eventually develop resistance to platinum-based treatment.
Platinum-resistant ovarian cancer is commonly defined as disease progression within six months of the last dose of platinum-based chemotherapy. Once disease reaches this point, treatment options are limited, response rates to standard single-agent chemotherapy have often been reported in the low double digits and benefits are usually short-lived. Patients may also have accumulated significant toxicities from earlier lines of systemic therapy, making tolerability a central concern alongside efficacy.
Director of Oncology
CureLab Oncology
CEO
CureLab Oncology
CureLab Oncology, a biotech company developing anti-cancer biologics, is exploring a DNA-based therapeutic strategy designed to influence the tumor microenvironment, support anti-tumor immune activity and enhance the effects of chemotherapy. Its lead clinical candidate, elenagen, is an investigational p62/SQSTM1-encoding plasmid DNA therapy designed to reshape the tumor microenvironment.
In a randomized Phase II study in platinum-resistant ovarian cancer, the investigational DNA-based immunotherapy was evaluated in combination with gemcitabine. The study, recently published in the International Journal of Gynecological Cancer and presented at the 27th Congress of the European Society of Gynaecological Oncology (ESGO 2026), reported median overall survival of 13 months with gemcitabine alone compared with 25 months with the addition of elenagen. The combination was also associated with a 59% relative reduction in the risk of death. Safety profiles were reported to be similar between arms, with no new toxicity signals.
To discuss the clinical and scientific implications of these findings, Xtalks spoke with Gabriel Levin, MD, a Gynecologic Oncologist at the McGill University Health Centre and Director of Oncology at CureLab Oncology, and Alexander Shneider, PhD, CEO of CureLab Oncology and inventor of the investigational DNA-based immunotherapy.
The Clinical Challenges of Platinum-Resistant Ovarian Cancer
For Dr. Levin, platinum resistance marks a difficult turning point in ovarian cancer care because it signals that the tumor has learned to escape one of the most effective treatment backbones available.
“Platinum-resistant ovarian cancer is an old definition of how the tumor is responsive to our usual backbone, which is platinum-based chemotherapy,” Dr. Levin explained. “It means that disease progressed within six months from the last dose of platinum-based chemotherapy.”
Once ovarian cancer becomes platinum-resistant, treatment options become substantially more constrained. According to Dr. Levin, response rates to later-line chemotherapy are often modest, generally in the low 15% range or less, and the benefit is usually short-lived.
“It’s difficult to treat those patients because once we define the cancer as platinum-resistant ovarian cancer, it means that the cancer has learned how to escape our most effective backbone therapy,” he said.
Patients have often already received multiple courses of systemic therapy by this point, and cumulative toxicities such as bone marrow suppression, alopecia and neuropathy can affect treatment tolerance and quality of life.
Dr. Levin noted that a large proportion of advanced ovarian cancers are not curable and recur after first-line therapy. Eventually, many patients reach a platinum-resistant stage, where treatment options are limited and care may move toward palliation.
“The unmet needs are more effective treatments and more tolerable treatments,” he said. “We need options that really improve overall survival, control the patient’s symptoms and are accessible and improve quality of life because it’s not only about prolonging lives, it’s also about living lives which are respectful and have some quality.”
He also emphasized the need for therapies that can be used broadly, rather than only in biomarker-selected populations. While precision oncology has created important advances, not all patients have actionable biomarkers, and platinum-resistant ovarian cancer remains an area where broadly applicable strategies are needed.
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What the Phase II Data Showed
The Phase II findings presented by Dr. Levin at ESGO 2026 evaluated CureLab Oncology’s investigational DNA-based immunotherapy in combination with gemcitabine for platinum-resistant ovarian cancer. The study compared gemcitabine alone with gemcitabine plus the investigational therapy.
The reported overall survival signal was notable: median overall survival was 13 months in the control arm compared with 25 months in the combination arm.
“The finding of the overall survival from the Phase II trial is overwhelming,” Dr. Levin said. “It’s unheard of, reaching an overall survival of 25 months in the setting of platinum-resistant ovarian cancer.”
For Dr. Levin, the result is important not only because of the magnitude of the survival difference, but also because it may suggest effects beyond short-term tumor control.
“Moving the needle from 13 months, which was the control arm, to 25 months is a huge signal and potentially meaningful change in how we can manage platinum-resistant ovarian cancer and not only delay progression, but also prolong the life of this patient,” he said.
He added that the effect may point to longer-term changes in the tumor microenvironment that could influence responses to later lines of therapy. However, he was clear that the findings require confirmation.
“It was only a Phase II trial, and it needs to be further verified in a Phase III randomized controlled trial,” Dr. Levin said.
No New Toxicity Signals Reported
In oncology, improvements in efficacy are often accompanied by added toxicity. This is especially important in platinum-resistant ovarian cancer, where patients may have already experienced substantial treatment-related adverse effects.
In the Phase II trial, safety profiles were reported to be similar between arms, with no new toxicity signals associated with adding CureLab Oncology’s investigational DNA-based immunotherapy to the chemotherapy backbone.
“We noticed that in our Phase II trial that patients had no additive toxicity from treatment with elenagen, which is highly unusual,” Dr. Levin said.
This is clinically relevant because patients with platinum-resistant ovarian cancer often need therapies that can extend survival without further compromising quality of life. If confirmed in larger studies, the lack of new toxicity signals could help inform future treatment protocols and combination strategies.
How the DNA-Based Immunotherapy Is Designed to Work
CureLab Oncology’s investigational therapy is a plasmid-based therapy encoding p62/SQSTM1. Dr. Shneider described the plasmid as a molecular envelope: a circular DNA structure that can carry a selected genetic sequence.
“Imagine you went to Staples and bought an envelope, a standard envelope. Then you can put into this envelope any sort of a letter,” Dr. Shneider said. “Now instead of an envelope which you buy at Staples, imagine a circular DNA, let’s call it a plasmid. So it’s the same envelope but on a molecular level.”
The selected gene was p62/SQSTM1. Dr. Shneider said the original hypothesis was immunological: because cancer cells overexpress p62, a plasmid encoding the gene could help train the immune system to recognize and eliminate cells producing too much of the protein.
“My original idea was to put in there a gene called p62, and the original hypothesis was to use this gene for purely immunological reasons,” he explained. “It would train our immunity to identify and eliminate those cells which have too much of this gene, too much of this protein.”
The choice of p62 was deliberate. According to Dr. Shneider, cancer cells are biochemically dependent on overproducing p62, meaning they cannot easily stop expressing it to escape immune recognition.
“My entire previous life in vaccinology taught me that you need to select such a target that the cancer cells would not be able to omit, would not be able to stop producing,” he said. “p62 is a protein which cancer cells cannot stop overproducing because they’re biochemically addicted to it.”
However, he said subsequent work showed the immune-targeting hypothesis was only one part of a more complex mechanism.
“Natural processes are always much more multifaceted, much more complex, much more exciting than we model them to be,” Dr. Shneider said. “Although my original idea was correct, it was just a small cherry on a big cake.”
Turning “Cold” Tumors “Hot”
A central scientific concept behind CureLab Oncology’s investigational therapy is its potential effect on the tumor microenvironment. Dr. Shneider pointed to “cold” tumors as one of oncology’s major challenges.
“One of the biggest problems in oncology today is so-called cold tumors,” Dr. Shneider said. “It means our immune cells cannot penetrate those tumors.”
By contrast, “hot” tumors are more accessible to immune cells and may be more responsive to immunotherapies, chemotherapy, radiation therapy or other approaches that depend partly on immune activation.
“What does our product do? It turns cold tumors into hot tumors,” Dr. Shneider said. “It opens molecular gates for specific entry of immune cells inside a tumor.”
This mechanism is one reason CureLab Oncology sees elenagen as a potential combination therapy rather than only a standalone intervention. Dr. Shneider said he expects it could eventually be used alongside chemotherapy, immunotherapy, radiation therapy and other cancer treatments.
Changing the Conditions Around the Tumor
Beyond helping immune cells enter tumors, elenagen is also being studied for its potential role in reducing chronic inflammation and preserving immune activity inside the tumor microenvironment.
“Tumors have ways to suppress immunity inside the tumor,” Dr. Shneider said. “What our product does, because it eliminates chronic inflammation, and chronic inflammation is a common denominator for all sorts of immune suppression within the tumor, we not only open the gates for immune cells to penetrate the tumor, but we also preserve activity of the immune response inside the tumor.”
This distinction is important because elenagen is not designed primarily as a direct cytotoxic attack on cancer cells. Instead, the company is exploring whether it can alter the tumor microenvironment in ways that make tumors more vulnerable to immune attack and more responsive to other therapies.
“We do it not by directly attacking cancer cells, but by changing the tumor microenvironment,” Dr. Shneider said.
How a Supply Disruption Informed Next Steps
One unusual aspect of CureLab Oncology’s clinical development story came from an unplanned supply disruption in July 2022. For non-medical logistical reasons beyond the company’s control, patients in the study had to stop receiving elenagen. Dr. Shneider emphasized that such an interruption would never have been introduced intentionally, as clinical ethics require patient interests to remain the top priority.
However, the disruption created an opportunity for retrospective analysis. At the time treatment stopped, some patients had received the investigational therapy for less than one month, while others had received it for several months or as long as 30 months.
This allowed the team to examine whether duration of exposure was associated with survival after treatment discontinuation.
“If we look retrospectively and see for how long a person received elenagen, can we predict for how long she will live or stay alive after elenagen was stopped from being administered?” Dr. Shneider said.
According to Dr. Shneider, mathematical analysis showed a strong relationship during the first 12 months of treatment: the longer patients received the investigational therapy, the longer they tended to live after stopping treatment. After 12 months, each additional month appeared to provide continued benefit, but the incremental benefit became progressively smaller. By approximately 18 months, the added benefit of each additional month appeared to be more limited.
This retrospective finding is informing future trial planning. Dr. Shneider said the company expects future courses of the investigational therapy to be somewhere between 18 and 24 months.
The insight also led the team to reconsider the magnitude of the reported Phase II result. Because the survival analysis included patients who received the investigational therapy for different durations, Dr. Shneider believes the published overall survival figure may underestimate the potential effect in patients who received longer treatment.
“It turned out that the results we report in our paper are a huge understatement,” he said. “If we look at only the patients who received it for over 18 months, the results were exceeding my most enthusiastic expectations.”
While these observations are encouraging, they remain exploratory and require prospective confirmation. Dr. Shneider said the team is also using the clinical observation to investigate the molecular, cellular and immunological basis of the time-dependent effect.
“We will not go just from science to a drug, but we will go from a drug to science,” he said.
Future Clinical Development in the US and Europe
CureLab Oncology has completed international Phase I/IIa clinical trials of elenagen and has initiated Phase II studies outside the US. Following proof-of-concept results generated outside the US, the company is preparing for additional clinical development in the US and Europe.
Dr. Shneider said the next step is to repeat and expand the findings with leading American clinical centers and key opinion leaders.
“We have achieved proof-of-concept results ex-US,” he said. “Now, in partnership with the best American clinical centers, which are very receptive to our work, we shall repeat it here in the United States.”
The company is proposing a Phase II/III development path in platinum-resistant ovarian cancer. According to Dr. Shneider, the planned approach would initially compare standard of care alone with standard of care plus elenagen in smaller patient groups, followed by expanded enrollment with more patients assigned to the investigational therapy arm than the control arm.
Dr. Shneider said that if larger trials reproduce the Phase II findings, the data could support discussions with regulators about an expedited development or authorization pathway.
The company is also planning to pursue development in aggressive forms of breast cancer, including triple-negative breast cancer. Over time, CureLab Oncology is considering additional cancers in which inflammation plays a role in disease biology.
Looking Beyond Oncology
Although CureLab Oncology’s current clinical priorities are focused on cancer, Dr. Shneider said the biology of chronic inflammation may eventually support development in other disease areas.
Based on preclinical, animal and human data, the company is considering future exploration beyond oncology, including chronic inflammatory diseases involving the central nervous system, metabolic disease and chronic pain.
For Dr. Shneider, these conditions may appear distinct clinically, but they can share common molecular and cellular roots.
“For a medical doctor, they’re different diseases, but to a molecular and cellular biologist, they are different plants growing from a common root, and the common root is chronic inflammation,” he said.
“A small biotech company should have its priorities focused,” he added. “We have strategic plans for the future, but we shall approach it on a step-by-step, frugal, responsible basis.”
A Tumor Microenvironment Strategy for a High-Unmet-Need Cancer
CureLab Oncology’s Phase II data introduce a potentially important clinical signal in platinum-resistant ovarian cancer, a setting where survival gains have historically been difficult to achieve and tolerability is a major concern.
By using a plasmid-based approach to encode p62/SQSTM1, CureLab Oncology is pursuing a strategy that aims to reshape the tumor microenvironment, reduce chronic inflammation, stimulate anti-tumor immune activity and enhance the effects of chemotherapy. The company’s scientific rationale is not simply to attack cancer cells directly, but to alter the biological conditions that allow tumors to evade immune control.
If confirmed in larger trials, CureLab Oncology’s approach could open a new path for platinum-resistant ovarian cancer treatment.
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