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"One way to think about how Anktiva works is it is the first molecule, based on the package insert, that increases and proliferates the NK cells, the T cells, and the CD4+ and CD8+ T cells, without up-regulating the suppressive T cells," says Patrick Soon-Shiong, MD.

Anktiva as a lymphocyte rescue molecule: Unlocking the power of NK cells and T cells

Dr. De La Cerda provides an overview of a patient case involving a 68 year-old male presenting with severe back pain, with an analysis of the clinical presentation, workup, and medical history.

Bone Predominant mCRPC Patient Case

Video content above is prompted by the following:

What are your initial impressions of the case?

Video Series

The FDA has accepted a Biologics License Application (BLA) seeking approval of nivolumab (Opdivo) co-formulated with Halozyme’s proprietary recombinant human hyaluronidase (rHuPH20), or subcutaneous nivolumab, for the treatment of patients with all previously approved solid tumor indications for nivolumab as a monotherapy, monotherapy maintenance following completion of combination therapy with nivolumab plus ipilimumab (Yervoy), or in combination with chemotherapy or cabozantinib (Cabometyx).

Nivolumab is currently approved under several indications, including in combination with ipilimumab for the first-line treatment of patients with intermediate- or poor-risk advanced renal cell carcinoma (RCC), in combination with cabozantinib for the first-line treatment of patients with advanced RCC, for the treatment of patients with advanced RCC who have received prior anti-angiogenic therapy, and in combination with cisplatin and gemcitabine for the first-line treatment of patients with unresectable or metastatic urothelial carcinoma.

The FDA is set to have a decision regarding the subcutaneous nivolumab formulation on or by December 29, 2024.

 According to a news release from Bristol Myers Squibb,

 approval of the formulation would make it the first and only subcutaneously administered PD-1 inhibitor.

“We believe subcutaneous nivolumab has the potential to make a significant difference in the lives of patients, which is reinforced by the FDA’s acceptance of our application,” said Gina Fusaro, PhD, vice president, global program lead, Bristol Myers Squibb, in the news release.

 “Opdivo is a foundational PD-1 inhibitor approved for many different types of cancer, and our continued investment in research that puts patients first remains a priority. If approved by the FDA, the subcutaneous administration of nivolumab would provide patients and their physicians with a new option that delivers the same well-known benefits as IV Opdivo but with the improved convenience of an injection administered in 3 to 5 minutes rather than a 30-to-60-minute infusion.”

The BLA submission is supported by findings from the phase 3 CheckMate-67T trial (NCT04810078), in which subcutaneous nivolumab met the study’s co-primary end points by demonstrating noninferiority to intravenous (IV) nivolumab regarding time average nivolumab serum concentration over 28 days (C

; geometric mean ratio [GMR}, 2.098; 90% CI, 2.001-2.200) and minimum serum concentration at a steady state (C

Data from the study, which were presented at the 2024 American Society of Clinical Oncology Genitourinary Cancers Symposium in San Francisco, California,

 also showed that subcutaneous nivolumab demonstrated noninferiority to IV nivolumab in the key powered secondary end point of objective response rate (ORR). Specifically, the subcutaneous arm demonstrated an ORR of 24.2% (95% CI, 19.0-30.0) per blinded independent central review (BICR), compared with 18.2% (95% CI, 13.6-23.6) in the IV arm.

The safety profile for subcutaneous nivolumab was consistent with that of the IV formulation. Among patients who received the subcutaneous formulation, 8.1% experienced injection-site reactions, with all being low-grade and transient. Deaths due to study drug toxicity occurred in 3 patients in the subcutaneous arm and 1 patient in the IV arm. Most deaths that occurred during the study were due to disease progression.

In total, the phase 3, open-label CheckMate-67T trial enrolled 495 patients with advanced or metastatic ccRCC who had received prior systemic therapy. Patients were randomly assigned 1:1 to receive 1200 mg subcutaneous nivolumab plus rHuPH20 every 4 weeks (n = 248) or to 3 mg/kg IV nivolumab every 2 weeks (n = 247) for up to 2 years of treatment or until disease progression, unacceptable toxicity, withdrawal, or death.

The co-primary pharmacokinetic end points for noninferiority testing were C

 of subcutaneous nivolumab vs IV nivolumab. The key secondary end point was ORR per BICR.

Final completion of the CheckMate-67T study is expected in January 2026.

1. U.S. Food and Drug Administration accepts Bristol Myers Squibb’s application for subcutaneous nivolumab (nivolumab and hyaluronidase). News release. Bristol Myers Squibb. May 6, 2024. Accessed May 7, 2024. https://news.bms.com/news/corporate-financial/2024/U.S.-Food-and-Drug-Administration-Accepts-Bristol-Myers-Squibbs-Application-for-Subcutaneous-Nivolumab-nivolumab-and-hyaluronidase/default.aspx

2. Bristol Myers Squibb announces updated action date by the U.S. Food and Drug Administration for subcutaneous nivolumab (nivolumab and hyaluronidase). News release. Published online and accessed May 21, 2024. https://investors.bms.com/iframes/press-releases/press-release-details/2024/Bristol-Myers-Squibb-Announces-Updated-Action-Date-by-the-U.S.-Food-and-Drug-Administration-for-Subcutaneous-Nivolumab-nivolumab-and-hyaluronidase/default.aspx

3. George S, Bourlon TB, Chacon MR, et al. Subcutaneous nivolumab (NIVO SC) vs intravenous nivolumab (NIVO IV) in patients with previously treated advanced or metastatic clear cell renal cell carcinoma (ccRCC): Pharmacokinetics (PK), efficacy, and safety results from CheckMate 67T. 

4. A study of subcutaneous nivolumab versus intravenous nivolumab in participants with previously treated clear cell renal cell carcinoma that is advanced or has spread (CheckMate-67T). ClinicalTrials.gov. Last updated March 1, 2024. Accessed May 7, 2024. https://clinicaltrials.gov/study/NCT04810078

The FDA is set to have a decision regarding the subcutaneous nivolumab formulation on or by December 29, 2024. 

News

FDA accepts BLA for subcutaneous nivolumab in solid tumors

Panelists explore challenges in identification of intermediate risk patients and emphasize importance of risk stratification to improve outcomes in regards to NMIBC.

Episode 2 Podcast: Identifying Patients with Intermediate Risk in NMIBC 

Advancing Patient Care in Non–Muscle-Invasive Bladder Cancer 

A panelist discusses how identifying intermediate-risk patients, managing disease heterogeneity in non–muscle-invasive bladder cancer, and addressing long-term care needs present key challenges in patient care while highlighting recent treatment advances that offer promising solutions.

Episode 1: Advancing Patient Care in Non–Muscle-Invasive Bladder Cancer

Matthew R. Cooperberg, MD, MPH, comments on disparities data highlighted in the recent Cancer Statistics, 2025 report from the American Cancer Society

Matthew Cooperberg, MD, on racial disparities in prostate, bladder cancer outcomes 

, comments on disparities data highlighted in the recent Cancer Statistics, 2025 report from the American Cancer Society. Cooperberg is a professor of urology and epidemiology & biostatistics at the University of California, San Francisco Helen Diller Family Comprehensive Cancer Center.

Prostate cancer has the greatest racial disparity in terms of excess mortality for Black compared to White patients of all the major human cancers. This has been observed and validated year after year, going back 25, 30 years. Black patients have over 2-fold excess mortality compared to White men, and that has been fairly consistent; the actual rate ratio has hovered between 2 and 2.5 for many years. It does seem to be potentially on a downtrend in the last couple years. This is partly because, at least in some contexts, we've been screening younger Black men a little bit more intensively, which is exactly the right thing to do if we want to address the mortality disparity. There's also been a lot of focus on this disparity for a lot of years in terms of research and trying to understand what drives it. The answer to that question, by the way, is it's complicated and it's multifactorial. There is clearly a genetic component, and we see this with global epidemiologic data. The highest rates of prostate cancer mortality in the world are seen in West and Southern Africa and in the Caribbean, specifically. So, this is not simply a reflection of social demographics or of human development index in the global epi data, but then you layer on to that all the social and structural determinants of health and structural inequalities that have persisted for decades, that exacerbate whatever genetic substrate we're dealing with.

It does not seem to be so much an access to care issue. When you look at screening rates, they actually have been comparable over many years. We don't really see treatment disparities in terms of getting access to surgery and radiation. From the point of diagnosis forward, outcomes really appear to be pretty much the same for Black and White men once you adjust for risk factors at the time of diagnosis. The story really appears to be upstream of diagnosis. There have been some nice modeling studies, again, from the CISNET group, who looked at the mortality downtrend and trying to understand the impact of screening. It's the same statisticians at Fred Hutch and Michigan and Erasmus, who concluded that the trajectory for prostate cancer is very similar in Black and White men, but the whole thing starts about 5 years earlier for Black men. This is the basis of the rationale for earlier screening for Black men, which is now formalized in the AUA screening guidelines [and] in the American Cancer Society [guidelines]. Pretty much all of them at this point, except for the US Preventive Services Task Force, recommend a 5 year earlier start for patients with risk factors; Black race, family history, any known genetic predisposition like 

, [all] would indicate starting earlier, maybe as early as 40.

When you look at some of the other cancers, you see other stories. [If] you look at bladder cancer, in this update here, it's a very different story. In bladder cancer, for reasons that are not particularly clear, in terms of the population mortality rate, it's actually a little bit lower for Black compared to White patients, but the outcomes after diagnosis are substantially worse. It's almost the opposite situation as in prostate cancer. In prostate, Black men are getting more and worse prostate cancer, but outcomes are similar once you've got the diagnosis; bladder cancer, it's the opposite. Again, for reasons that are not clear, there seems to be less lethal disease at the population level, but outcomes are substantially worse from diagnosis forward, which tells us there we really do have an access to care and quality of care challenge to take on.

This transcript was AI generated and edited by human editors for clarity.

“Black patients have over 2-fold excess mortality compared to White men, and that has been fairly consistent; the actual rate ratio has hovered between 2 and 2.5 for many years,” says Matthew R. Cooperberg, MD, MPH. 

Matthew R. Cooperberg, MD, MPH, highlights key prostate cancer data from the American Cancer Society’s Cancer Statistics, 2025 report 

Matthew Cooperberg, MD, reacts to 2025 ACS prostate cancer data

, highlights key prostate cancer data from the American Cancer Society’s 

 report and considers the causes of the rise in incidence and mortality. Cooperberg is a professor of urology and epidemiology & biostatistics at the University of California, San Francisco Helen Diller Family Comprehensive Cancer Center.

These are, first of all, incredibly helpful data, and it's wonderful that the American Cancer Society puts so much effort into compiling them every year. Every year in January, everybody's waiting to see what the updates are going to look like. It's been a really great source of insights into the trends over time that we've seen in, of course, all cancers—we're focusing on prostate today specifically—but it's really an amazing resource. There's a paper published every year and a companion, longer document Cancer Facts and Figures that I think defines a lot of what we do in terms of year-to-year epidemiology in the US for all cancers.

The prostate update this year is that the expectation for 2025 is over 313,000 men will be diagnosed with prostate cancer, and over 35,000 will die of the disease. These numbers are going up, and they're going up at a significant clip. Every year these data are updated. There's a lot of discussion about what is driving the trends. It really goes to the complexity of tracking prostate cancer epidemiology in terms of both incidence and mortality for the reasons that incidence of prostate cancer is so tightly tied up with screening and how hard we are looking for prostate cancer and how we're defining prostate cancer. Mortality, in turn, typically takes literally decades after diagnosis to occur when it is going to occur. So, when we look at the incidence data year to year, what we're really looking at is intensity of screening and diagnostic endeavors, which start at the primary care level. When we look at the mortality data, we're looking at the effects of policy decisions that we made years ago and in some cases, decades ago.

Of course, the elephant in the room when we talk about these trends over the last 20 years in prostate cancer is screening patterns and the impact of the US Preventative Services Task Force in particular over the years. The trend, as we've seen it unfold, is that when prostate cancer screening first hit the marketplace and hit attention in the early 2000s, prostate cancer incidence rates skyrocketed because we identified all these prevalent cases. All these men who had been living with asymptomatic prostate cancer in the pre-screening era, we suddenly found all these cancers, and there was a huge spike in incidence to the highest rates we have ever seen before or since. Then things stabilized throughout the 90s and 2000s as screening became more popular. Then, of course, with recognition of overtreatment and some very deeply flawed interpretations of the emerging trial literature, the US Preventive Services Task Force recommended in 2008 that we stopped screening men over 75, and in 2012 they said we should stop screening all men, period. They had a lot of prevaricating language in the guideline, but at the end of the day, that's what they said, and that is what primary care docs interpreted. Literally, overnight, screening rates fell 25%. The incidence rates following 2012 fell to the lowest level we've seen since the 1980s. It's not because prostate cancer disappeared, it's because we literally stopped looking for it. Then, in 2018, at least in part, recognizing that we are now doing active surveillance and we're trying not to treat low-risk prostate cancer. We got this C recommendation from the Task Force, which is saying, "Well, we still don't really recommend this, but you should have a conversation with men". The incidence rate is going up again because screening rates have started coming up again. I think a lot of us have the sense that now we really know how to do smarter screening and treatment to a much better extent than we did before.

So, that's the incidence story. In the meantime, the mortality story, death rates for prostate cancer had been falling consistently since the 1990s, the early years of the screening era. They fell throughout the 90s and 2000s at a faster velocity than any other cancer except lung cancer. We know the setting in the case of lung cancer, this is obviously because of smoking cessation. Less smoking across the population, that is clearly what drives the mortality drop for lung cancer. In the case of prostate cancer, it was controversial for a lot of years how much of this could be attributed directly to screening. The best analyzes from the CISNET group suggests that it's at least a third, and then another third can be attributed to improvements in treatment for high-risk localized disease. Some of it may be smoking for the case of prostate cancer as well. It is a smoking-related tumor, not as obviously as bladder and kidney cancer are. There are other epidemiologic factors as well, but there's no question that a lot of this drop we can credit to screening. The mortality declines pretty much flattened out as of 2013-2014.

Now that was a little bit too soon to blame it directly on the 2012 US Task Force D recommendation. There are probably some other factors that are tending to drive prostate cancer mortality increases. Part of it is just the aging male population, less early cardiac death. There are secular trends out there, but I think we can say it was the worst possible time to stop screening. Mortality rates started ticking up a little bit. They're mostly flat for the current year, but it does seem clear that we need to get back to a smarter middle ground of screening—using screening more intelligently, finding the high-grade cancers and treating them—so that we can get that mortality curve back on a downward trajectory.

Prostate cancer incidence and mortality are rising, with over 313,000 diagnoses and 35,000 deaths expected in 2025. Screening practices significantly influence these trends, as seen with the US Preventive Services Task Force's recommendations, which led to fluctuating screening rates and incidence. Mortality rates, which had been declining since the 1990s, have plateaued, partly due to aging populations and past policy decisions. A balanced approach to screening, focusing on high-grade cancers, is crucial to reducing mortality and improving outcomes in prostate cancer management.

“It does seem clear that we need to get back to a smarter middle ground of screening—using screening more intelligently, finding the high-grade cancers and treating them—so that we can get that mortality curve back on a downward trajectory,” says Matthew R. Cooperberg, MD, MPH. 

Patrick Soon-Shiong, MD

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