Immuno-oncology roundup

A roundup of recent research and deal-making news in the field of immuno-oncology, as well as a bonus guest commentary from Novella Clinical

Register for free to listen to this article
Listen with Speechify
The first of their kind
Researchers test a new immunotherapy combo and a pioneering approach to cancer vaccination
By Mel J. Yeates & Jeffrey Bouley
Signaling double trouble for some cancers, researchers in Augusta, Ga., have paired two immunotherapies together as a novel way to tackle tumors. Specifically, pembrolizumab, which enables the T cells a patient already has to better attack a tumor, and poly-IC, which can produce an independent and vigorous immune response, are being given together for the first time to help more patients wage a stronger war on a wide range of solid tumors, researchers say.
The first phase of the clinical trial of this unique pairing is looking at the safety of combining the two drugs in a dozen patients with solid tumors, like lung or liver cancer, which have not responded to standard therapy. A second phase will commence at its completion in about 30 patients with nonresponsive metastatic colon cancer.
“We have experiments in mice that show that the combined use of PD-1 antibody and poly-IC is synergistic for the recognition of tumors and an antitumor response mediated by T cells,” noted Dr. Esteban Celis, co-leader of the Cancer Immunology, Inflammation and Tolerance program at the Georgia Cancer Center at Augusta University. 
“Now we want to see if this synergy can also work for patients,” added Dr. Sharad Ghamande, associate director for clinical research and trials at the Georgia Cancer Center—as well as chief of the Division of Gynecologic Oncology and executive vice chair of the Department of Obstetrics and Gynecology at the Medical College of Georgia. Ghamande is principal investigator on the first trial. Dr. Asha Nayak-Kapoor, hematologist/oncologist at MCG and the Georgia Cancer Center, will lead the colon cancer trial.
Celis’ lab has shown how poly-IC, which behaves like the genetic material of viruses to get the attention of the immune system, can improve the effectiveness of therapeutic cancer vaccines. During those studies, he found the synergy between these two immunotherapy agents as well.
PD-1 is a molecule naturally expressed by T cells, a type of white blood cell that can fight infections and cancers, to help prevent an overzealous immune response. But tumors have a ligand for the molecule, called PD-LI, and their interaction inhibits the activity of the T cells that kill tumors, Celis explained.
“The antibody blocks the interaction and allows those T cells that are already at the tumor site to be more effective,” he noted. The synthetic PD-1 antibody, pembrolizumab, is already used by physicians to help treat a wide range of cancers by releasing the brakes on T-cells that recognize tumors, Celis added.
But a caveat is that many patients have few if any T cells in their tumors, which means the treatment is effective in only about 20 percent of patients who also have high microsatellite instability. That means that their tumor has a lot of genetic mutations, which are likely to get the attention of the immune system despite scarce T cells. These tumors are characterized as immunogenic.
“The idea is that tumors that have a lot of mutations are more immunogenic, so that is why they tend to be infiltrated by T cells,” Celis said. “In tumors that are less immunogenic, we hope that Poly-IC will make them more immunogenic.”
In other unique immuno-oncology news—and going “across the pond” to Europe—a first-of-its-kind treatment vaccine has moved into a Phase 1 clinical trial for patients with non-small cell lung cancer (NSCLC), under a collaboration agreement between Cancer Research UK and Asterias Biotherapeutics Inc.
Cancer Research UK will manage the initial clinical development of AST-VAC2, which it describes as “a promising immunotherapy candidate derived from a standardized human embryonic stem cell line.”
If shown to be safe and effective, the hope is that AST-VAC2 could serve as an additional treatment for patients who no longer have advanced disease but whose lung cancer is at high risk of returning. Also, it could possibly be of use in combination with other treatments for patients who have advanced disease.
“This vaccine trial is a pioneering approach to improving treatment for lung cancer, the biggest cause of cancer death worldwide,” said Dr. Nigel Blackburn, Cancer Research UK’s director of drug development. “By coupling our expertise with a leading biotechnology company, we’ve accelerated the development of this experimental treatment by years.”
The vaccine is made from dendritic cells that are able to “kick-start” the body’s immune system, according to Cancer Research UK—they present antigens on their surface and orchestrate a T cell immune response against cells bearing the same antigens. AST-VAC2 dendritic cells are engineered to express a modified form of a protein called telomerase, which is almost always present at high levels in various types of cancer cells, but rarely found in healthy cells.
This modified form of telomerase, called hTERT, can stimulate a natural immune response targeted at cancer cells. High levels of telomerase are a common feature of many cancers, so AST-VAC2 has the potential to become an immunotherapy option for other types of cancer beyond NSCLC, according to the collaborators.
Previous dendritic cell therapies have been made using patients’ own cells, but this process is costly, slow and inefficient. By using a pioneering approach of growing mature dendritic cells from a single human embryonic stem cell line in the laboratory, it’s hoped AST-VAC2 will overcome these challenges.
Michael Mulroy, president and CEO of Asterias, said: “The experience and expertise of Cancer Research UK’s Centre for Drug Development and Biotherapeutics Development Unit have brought us a step closer to realizing the clinical potential of this exciting experimental treatment ... In the future, there’s also the potential to utilize this novel platform technology to produce treatments that could, in theory, target multiple tumor antigens and thereby treat a whole range of different cancers and tumor types.”

Commentary: Immuno-Oncology—Gold Rush or a Golden Age?
By Dr. Andy Kinley of Novella Clinical
The last few years saw the success of checkpoint inhibitor drugs like pembrolizumab and nivolumab in treating cancer and brought on a whole new meaning to the field of immunotherapy. Modulating the immune system to kill tumor cells became a main focus of many drug sponsors and the term “immuno-oncology” became a new buzzword. Estimates show1 that currently hundreds of clinical trials involving immuno-oncology therapies are being carried out with the recruitment of over a hundred thousand patients.
As excitement builds in the field, concerns have also arisen about poorly designed trials, patient safety and inefficient use of research funds and patient volunteers. In this commentary, we take a deeper look at the status of the crowded immuno-oncology field and explain how drug sponsors (and the scientific world in general) can derive the best benefit from a multitude of clinical trials and the information so gathered.
A feverish hype has surrounded the field of immuno-oncology (IO) over the past decade with the discovery and approval of several checkpoint inhibitors. Keytruda (pembrolizumab), perhaps the most notable checkpoint inhibitor, has been approved for the treatment of melanoma, lung cancer, head and neck cancer and several other cancer types.
The concept of cancer immunotherapy is not new, and the beginnings of the field can be traced back to findings made more than a century ago. However, incredible progress has been made recently, and with the success of drugs like Keytruda, which generated greater than $1 billion in sales in the third quarter of 2017 alone, the business case for industry focus on immuno-oncology therapeutics is clear.
Is IO experiencing a gold rush?
Keytruda is one of six FDA-approved checkpoint inhibitors2 for the treatment of a wide variety of cancers. Due to their market and medical success, there has been great interest from both academia and pharmaceutical companies in these classes of drugs. This interest has translated into a populous drug development pipeline for cancer immunotherapeutics: 50 checkpoint inhibitors are being evaluated in 1,502 studies, 1,105 of which are in combination with other treatments.3 Thought leaders in the field, however, have criticized the massive number of trials, calling it a “gold rush”4 with pharmaceutical companies seeking to take advantage of the clinical and commercial success of these drugs.
Do these criticisms hold merit? Many claim that this rush has led to hastily planned trials that lack sufficient scientific rationale and/or preclinical investigation. These types of trials, as experts note, do not advance our scientific understanding of how these therapeutics work or cancer’s ability to develop resistance. The failed ECHO-301 study5 of IDO inhibitor epacadostat in combination with pembrolizumab in advanced melanoma is often highlighted as an example of rushing into a (Phase 3) clinical trial without robust early-phase and efficacy data.
One additional criticism of the excessive number of trials being run is that they are quickly exhausting oncology’s most precious and important resource—eligible patients.6 Many trials call for a very specific patient type—patients who have relapsed, are in a specific stage or have a specific biomarker—and enrolling them in trials that are essentially testing similar drugs could make it difficult for other trials studying more innovative and novel therapies to find enough subjects.
So, it may be worth asking the question: Since there are already six FDA-approved checkpoint inhibitors, five of which inhibit the same PD-1 signaling pathway, do patients really need additional treatment options that have a similar mechanism of action?
Not a gold rush, but a golden age?
Answering this question, like studying cancer, is no easy task. Cancer is a complex disease capable of altering a patient’s immune system in a variety of ways. While researchers and clinicians have gained deep insights over the past century, there are still many unanswered questions. Preclinical research and tumor models can help to answer some of these questions; however, they may not be a good predictor of safety or efficacy in humans. Thus, performing well-designed clinical trials allows researchers to formulate a more unifying hypothesis for how different cancers, and the immunotherapies that treat them, work.
For this reason, other thought leaders in immuno-oncology have taken a view opposing those criticizing the “gold rush,” calling the current era a “golden age of oncology drug development.”7 Only 10 to 30 percent of patients respond to checkpoint inhibitors, and with the extraordinary cost of drugs like Keytruda, which is priced at $150,000 a year, it seems there is plenty of room for innovation to create more effective drugs, or combinations, that are cheaper for patients.
In addition, some of the critiques of the IO “gold rush” may not be 100-percent accurate. With the massive number of trials and the seemingly small number of eligible patients, it is easy to believe that patients are being enrolled in trials that will not necessarily provide additional information or simply repeat similar studies. However, about 60 percent of the 1,500 studies mentioned above are small, single-site trials. Many of these are dose-escalation or expansion studies, and while they can expand to include a large number of patients, typically enrollment is gated, based on preliminary safety and efficacy data. These exploratory trials usually involve only 15 to 20 patients in each treatment arm and will not expand to enroll more. Therefore, trial databases may artificially overestimate patient demand.
One additional argument for companies developing their own PD-L1 inhibitors is financial. PD-L1 inhibitors are the foundation for the treatment of many types of cancer. Their continuously growing success in a variety of indications and their use in combination with other treatments means that any emerging company looking to break into the immunotherapy market will either need to partner with large pharmaceutical companies with approved PD-L1 therapies, or develop their own checkpoint inhibitor.
Beyond checkpoint inhibitors to novel therapies
The crowded IO field can also lead to the development of innovative new approaches for the treatment of cancer. A few years ago, researchers proposed a framework called the Cancer-Immunity Cycle8 for thinking about the steps by which immune cells (specifically T cells) are primed to attack cancer cells, infiltrate the tumor microenvironment,9 recognize which cells are cancerous and kill them. This framework has helped researchers identify new targets and pathways that could be exploited by novel cancer therapeutic strategies.
Many inventive companies have done just that, exploring second- and third-generation therapies. Some of these are a new wave of checkpoint inhibitors, either antibodies or small molecules, that “release the brakes” of the immune system by inhibiting molecules which prevent immune attacks against cancer cells (i.e., TIM-3, VISTA, LAG-3, IDO or KIR). Simultaneously, there is also active research into molecules that “step on the gas” by stimulating cellular targets (i.e. CD40, GITR, OX40, CD137 and ICOS) to kill cancer cells. 
A gold standard
With the hype and activity in the immuno-oncology field increasing, there are sure to be additional successes and failures, adding fuel to the fire for each side of this argument. One thing that both sides can agree on is that clinicians and researchers want clinical trials to be run with solid, scientific rationales that have the greatest potential to benefit patients. As we’ve described above, there is certainly a “gold rush” in the field, but it may not be as bad for patients as some have pointed out. The activity in this area has helped, and will continue to help, answer critical research questions and push revolutionary cancer therapeutics to market.
Andy Kinley, Ph.D., is senior director of oncology strategy at Novella Clinical, where he provides strategic guidance to the oncology and operational teams as well as consultative oversight for biopharma sponsors developing cancer therapeutics.

A bifunctional immunotherapy
Germany’s Merck KGaA presents updated clinical results for M7824 at ASCO meeting
DARMSTADT, Germany—In early June, Merck KGaA—based in Darmstadt, Germany, and traditionally known as EMD in the United States and Canada to distinguish it from Merck & Co.—announced results from expansion cohorts of the ongoing M7824 Phase 1 clinical trial program at the American Society of Clinical Oncology (ASCO) 2018 Annual Meeting in Chicago.
These data include results in patients with advanced non-small cell lung cancer (NSCLC) and in human papillomavirus-associated cancers, presented in collaboration with the National Cancer Institute, providing further evidence that bringing together a transforming growth factor-β (TGF-β) trap with the anti-PD-L1 mechanism may generate clinically relevant antitumor activity.
“M7824’s dual approach to fighting cancer, which brings together a TGF-β trap with the anti-PD-L1 mechanism, complements our existing immuno-oncology portfolio,” said Dr. Luciano Rossetti, global head of research and development at the biopharma business of Merck KGaA. “The unique design of this fusion protein offers the potential to optimally engage the TGF-β pathway. This is one example of the creative approaches we are taking to address challenging cancers where we believe we can deliver a transformational change for patients.”
In patients with second-line (no prior immunotherapy) advanced NSCLC from the cohort of the ongoing Phase 1 clinical trial, signs of clinical activity were seen across PD-L1 expression levels. At the recommended Phase 2 dose (1,200 mg every two weeks), an investigator-assessed confirmed overall response rate of 40.7 percent (11 of 27 patients) was observed. In patients with high PD-L1+ expressing tumors, ORR was 71.4 percent (five of seven patients). A median progression-free survival (PFS) of 6.8 months was observed for PD-L1+ patients (1,200 mg every two weeks), and the median PFS was not reached for the high PD-L1-expressing population, owing to the number of patients still responding at the time of analysis.
These data build on a number of recent readouts for M7824, including preliminary data in gastric cancer at the ASCO 2018 Gastrointestinal Cancers Symposium. Merck KGaA will present data from additional cohorts in hard-to-treat cancer types in the coming year.

Survivin research opens up new avenues for cancer immunotherapy
BUFFALO, N.Y.—New research from Roswell Park Comprehensive Cancer Center and MimiVax LLC shows that one of the most commonly occurring molecules in cancer cells may be an attractive target for a broad range of immunotherapy approaches, including CAR-T therapy. The study, “Survivin Monoclonal Antibodies Detect Survivin Cell Surface Expression and Inhibit Tumor Growth in vivo,” was published in March in Clinical Cancer Research, a journal of the American Association for Cancer Research.
Survivin is a cell-survival protein highly expressed by many types of cancer, including many glioma, lung, pancreatic, breast and neuroendocrine tumors and some forms of multiple myeloma, lymphoma and leukemia. Emerging vaccine approaches developed at Roswell Park and targeting the survivin protein may be more effective than standard therapy alone for some patients with glioblastoma.
Previously, survivin was thought to be present only inside the cancer cell, where some types of immunotherapy could not reach it. This preclinical study is the first to report that survivin can be found on the surface of cancer cells, which means that certain forms of immunotherapy targeting the protein could be effective against cancer cells. This observation suggests that antibody-based treatment approaches, including survivin CAR-T cell therapy, could be used to target both solid and liquid tumors—a finding that could help broaden the applications for CAR-T therapies.
“We’ve shown through our clinical trials of SurVaxM immunotherapy that survivin-targeting vaccines will stimulate both T-lymphocyte and antibody responses against survivin,” said senior author Dr. Michael Ciesielski, an assistant professor in the Department of Neurosurgery at Roswell Park. “Through this latest study, we have now discovered that antibodies that target cell-surface survivin have distinct therapeutic potential.”

Positive clinical data shared for DeCidE1 vs. ovarian cancer
HALIFAX, Nova Scotia—June also brought news that IMV Inc. shared new positive data in an oral presentation for its DeCidE1 (DPX-Survivac with low-dose CyclophosphamIDe and Epacadostat) clinical study at the 2018 American Society of Clinical Oncology annual meeting. These data from the ongoing Phase 1b/2 trial evaluated the safety and efficacy of the combination of IMV’s lead candidate DPX-Survivac and low-dose cyclophosphamide, with Incyte’s IDO1 enzyme inhibitor epacadostat, in patients with advanced recurrent ovarian cancer.
DPX-Survivac consists of survivin-based peptide antigens formulated in IMV’s proprietary DPX drug development platform. DPX-Survivac is believed to work by eliciting a cytotoxic T cell immune response against cells presenting survivin peptides. Survivin, recognized by the National Cancer Institute as a promising tumor-associated antigen, is broadly overexpressed in most cancer types and plays an essential role in antagonizing cell death, supporting tumor-associated angiogenesis and promoting resistance to anti-cancer therapies. IMV has identified over 15 cancer indications in which the over-expression of survivin can be targeted by DPX-Survivac.
During the presentation, Dr. Oliver Dorigo, an associate professor of obstetrics and gynecology (oncology) at Stanford University Medical Center, provided an update on the clinical benefits from the first 18 evaluable participants among 26 enrolled (including 10 from 100 mg epacadostat dosing cohort and eight from 300 mg epacadostat cohort), as well as blood sample and tumor biopsy analyses from the study’s first dosing cohort. IMV is conducting the Phase 1b/2 trial in an ongoing collaboration with Incyte Corp.
“We continue to be impressed by the safety and efficacy signals we see from this clinical trial, especially in this heavily pre-treated patient population with advanced ovarian disease and very limited treatment options,” said Frederic Ors, CEO of IMV Inc. “We designed DPX-Survivac to program immune cells in vivo in order to heighten and sustain anticancer T cell responses. Thus, we are especially pleased to be able to demonstrate, for the first time, a clear correlation between partial regressions and T cell infiltration in the tumors.”
At the time of data cut-off, 39 patients were enrolled (including 25 new participants in the 300mg cohort, with eight evaluable from day 56 first CT scan). Data from the first 18 evaluable patients across both dosing cohorts showed seven tumor regressions, including four partial responses (PR) reported so far (defined as ≥30-percent decrease in tumor lesion size). Study participants generally tolerated treatments well, with no related significant adverse events reported.            
Data from the first eight evaluable participants in the 300 mg epacadostat dosing cohort at first CT scan included six patients demonstrating stable disease at day 56, with four still on trial at data cut-off. Two patients with tumor regressions were observed so far, including one PR with a tumor regression ongoing for more than nine months. IMV plans to report updated results on these patients and others when data from at least 16 evaluable participants in the second dosing cohort are available.
Researchers also analyzed patient data to study the combination’s mechanism of action. They examined blood samples and tumor biopsies for the 10 evaluable patients treated in the first dosing cohort. These data showed that survivin-specific T cell responses were detected in 100 percent of patients. There was an increase in T cell infiltration post-treatment in 37 percent of the analyzable tumor biopsies based on two complementary testing methodologies (RNA sequencing and immunohistochemistry). Two of the three patients with T cell infiltration showed PRs with significant and durable tumor regressions lasting more than one year. The third patient with T cell infiltration exhibited progressive disease with evidence of downregulation of the major histocompatibility presentation pathway and significant increases in suppressive markers, both indicative of mechanisms of resistance.
“We know how important T cells are to controlling gynecological cancers, particularly in advanced ovarian disease, where it has been estimated that less than 20 percent of patients are responsive to monotherapies like checkpoint inhibitors,” said Dr. Gabriela Nicola Rosu, chief medical officer at IMV Inc. “IMV’s approach to program T cells in vivo is showing promising results that have been able to connect the dots between T cell infiltration and tumor response in these patients, many of whom have rapidly growing tumors. We believe this data is an important milestone toward our goal of significantly increasing the number of individuals able to benefit from immunotherapy treatments.”

Immune-stimulating cells shrink breast tumors
WEST VANCOUVER, British Columbia—A research team at BriaCell Therapeutics Corp., an immuno-oncology focused biotechnology company with a proprietary targeted immunotherapy technology, recently published a paper that sheds light on the potentially unique mechanism of action of BriaCell’s lead product candidate, Bria-IMT, in the journal Frontiers in Immunology.
The paper, titled “SV-BR-1-GM, a Clinically Effective GM-CSF-Secreting Breast Cancer Cell Line, Expresses an Immune Signature and Directly Activates CD4+ T Lymphocytes,” focuses on the mechanism of action of Bria-IMT, also referred to as SV-BR-1-GM, and may explain the impressive early clinical data on tumor shrinkage observed in some patients with metastatic breast cancer.
As summarized in the peer-reviewed publication, a body of evidence suggests immune-stimulating actions of SV-BR-1-GM which the paper’s authors believe are unique to Bria-IMT compared with other similar approaches. Bria-IMT (SV-BR-1-GM), the company’s lead product candidate, is derived from a specific breast cancer cell line. It is genetically engineered to release granulocyte-macrophage colony-stimulating factor (GM-CSF), a substance that activates the immune system, and the compound is thought to help the body recognize and kill tumor cells by activating both T cells that directly attack tumor cells, and, potentially, B cells that produce antitumor antibodies.
Specifically, Bria-IMT contains several factors, including HLA Class II molecules, molecules which typically are involved in starting an immune response. These molecules directly activate CD4+ “helper” T cells, a key component of the immune system, which can produce a strong immune response against tumor cells resulting in tumor size reduction also known as clinical regression. Complete or even partial regressions are difficult to achieve in advanced breast cancer patients who have failed the standard of care. BriaCell has previously reported such responses in patients with metastatic breast cancer, not only in soft tissue and visceral areas, but even in the brain, a difficult site to treat.

Medigene expands TCR alliance with bluebird bio
PLANEGG, Germany—Medigene AG recently announced a significant expansion of its successful strategic alliance with bluebird bio, a leader in gene and cell therapies, focusing on the research and development of T cell receptor-modified T cell (TCR-T) immunotherapies for the treatment of cancer.
“We are delighted to broaden this outstanding collaboration for the joint research and discovery of TCR lead candidates designed for the treatment of multiple cancer indications. Medigene is contributing its unique TCR technology platform, which encompasses multiple innovative screening and assessment tools to identify and characterize specific, non-modified TCRs to selected target antigens in a highly competitive timeframe.” said Dolores J. Schendel, CEO and chief scientific officer of Medigene. “The expansion of this alliance further validates the efficiency and quality of Medigene’s TCR platform technology.”
“As we continue to build our leadership in immuno-oncology, we value Medigene’s TCR technology platform which enables us to tackle intracellular tumor antigens not addressable by CAR-Ts,” added Dr. Philip Gregory, chief scientific officer of bluebird bio. “Our expanded collaboration will help us broaden our pipeline of TCR lead candidates for potential future clinical development.”
Under the revised terms of the agreement, the number of target antigen/MHC restriction combinations for the discovery of specific TCR lead candidates by Medigene will be increased from four to six. As part of this contractual expansion, Medigene will receive an additional one-time payment of $8 million. R&D funding for all work performed by Medigene in this collaboration will grow proportionally to address the broader scope of the collaboration. In addition, the aggregate amount of all potential development and commercial milestones as well as royalty payments has been significantly increased in line with the extended number of TCR projects.
If successfully developed and marketed through several indications and markets, Medigene could receive up to $250 million in milestone payments per TCR program in addition to tiered royalty payments on net sales up to a double-digit percentage. Following the amendment of the agreement, Medigene anticipates receiving an additional payment of $1 million associated with the first collaboration project under the agreement.
Based on the terms of the agreement signed in September 2016, Medigene is responsible for the discovery of TCRs for each target antigen selected by bluebird bio using its TCR technology platform. Following the collaborative non-clinical development, bluebird bio will assume sole responsibility for preclinical and clinical development and commercialization of the TCR-T cell product candidates and will receive an exclusive license for the intellectual property covering the selected TCRs.

Demonstrating response of IL-12 platform in breast cancer and glioblastoma
BOSTON—Ziopharm Oncology Inc., a biotechnology company focused on development of next-generation immunotherapies utilizing gene- and cell-based therapies to treat patients with cancer, in June presented clinical data showing the company’s Controlled IL-12 platform as monotherapy achieved antitumor responses in patients with metastatic breast cancer (mBC) and patients with recurrent glioblastoma (rGBM) at the 2018 American Society of Clinical Oncology Annual Meeting.
The poster, “Demonstration of Anti-Tumor Immunity via Intratumoral Regulated Platform Ad-RTS-hIL-12 in Advanced Breast Cancer and Recurrent Glioblastoma Patients,” presented data from two open-label trials that evaluated Ad-RTS-hIL-12 plus veledimex, a gene therapy designed to induce and control the expression of the powerful cytokine interleukin 12 (IL-12). Updated data from the company’s Phase 1 rGBM study shows median overall survival (mOS) of 12.7 months has been sustained for patients treated with Ad-RTS-hIL-12 plus 20 mg of veledimex at a mean follow-up time of 12.9 months as of May 4, 2018. This mOS of 12.7 months continues to compare favorably to the five to eight months survival established in historical controls for patients with rGBM.
“We remain excited that Ad-RTS-hIL-12 plus veledimex as monotherapy demonstrates promising antitumor responses and makes cold tumors hot with new immune-infiltrating cells and overexpression of checkpoints,” said Dr. Francois Lebel, Ziopharm’s chief medical officer and executive vice president for research and development. “We look forward to further development of our Controlled IL-12 platform in combination with immune checkpoint inhibitors, with one combination trial initiated in brain cancer and plans to advance a similar treatment regimen in a second tumor type later this year.”

Published In:

Subscribe to Newsletter
Subscribe to our eNewsletters

Stay connected with all of the latest from Drug Discovery News.

March 2024 Issue Front Cover

Latest Issue  

• Volume 20 • Issue 2 • March 2024

March 2024

March 2024 Issue