Abstract
Enzalutamide is an oral androgen receptor signaling inhibitor used in the treatment of prostate cancer. Elderly patients with prostate cancer commonly have age-related comorbidities that require concomitant, active treatment. As a moderate inducer of the cytochrome P450 (CYP) enzymes CYP2C9 and CYP2C19, and a strong inducer of CYP3A4, there is potential for drug-drug interactions (DDIs) when enzalutamide is coadministered with other drugs that are CYP3A4 substrates—resulting in loss of efficacy or increased risk of unintended drug-related adverse events. In this podcast, we describe enzalutamide including its dosing, pharmacokinetics, and potential for interaction with coadministered drugs using several hypothetical patient cases with real-world clinical implications. Discussion of each patient case will highlight management strategies and illustrate that nearly all enzalutamide drug-drug interactions can be effectively managed with appropriate knowledge of which drugs pose interaction risks, when dose adjustments are indicated, and when alternative drugs can be substituted.
Supplementary file1 (MP4 192541 KB)
Supplementary Information
The online version contains supplementary material available at 10.1007/s40264-025-01600-2.
Key Summary Points
| Enzalutamide is a prostate cancer treatment that can interact with other medications, especially those processed by certain liver enzymes (CYP3A4, CYP2C9, and CYP2C19). |
| These drug-drug interactions (DDIs) can reduce the effectiveness of medications or increase the risk of side effects. |
| Proper management, including dose adjustments or switching medications, can help minimize these interaction risks. |
Podcast Audio
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Podcast Transcript
Judeth Bianco: Hello and welcome. I’m Judeth Bianco from Pfizer Inc.
Jesse Mack: And I’m Jesse Mack from Astellas Pharma. We’re both clinical pharmacists by training and your hosts for today’s podcast on Managing Drug Interactions With Enzalutamide in Patients With Prostate Cancer—available in the journal Drug Safety. Editorial support for this podcast was provided by Jack Liao, PhD, at Impact Communication Partners and funded by Pfizer and Astellas Pharma. The patient cases described in this podcast are fictional and do not represent actual events or a response from actual patients. The authors developed fictional cases for educational purposes only.
Judeth Bianco: In this podcast, we’re diving into the complex world of prostate cancer treatments and the risk of drug-drug interactions, a situation that can happen when patients take several concurrent medications for various comorbid conditions.
Jesse Mack: We’re happy to have Dr. Alicia Morgans from the Dana-Farber Cancer Institute and Dr. Brooke Looney from the Vanderbilt University Medical Center to share their insights and expertise on this important topic. Thank you both for joining.
Alicia Morgans: Thank you so much Jesse and Judeth for having me. I’m so happy to be here. Actually, I just want to share that I’m a GU medical oncologist with a focus for most of my patient care in prostate cancer and again just very happy to be here.
Brooke Looney: Thank you Jesse and Judeth, I’m thrilled to be here as well. I am a clinical pharmacist with the adult outpatient oncology specialty pharmacy at the Vanderbilt University Medical Center where my primary focus is on oral oncology medications, and that ranges from access and affordability, to patient education, monitoring, and outcomes research.
Judeth Bianco: It’s great to talk with both of you again. Let’s take a minute and discuss why we’re here and why this is so important for our listeners: Prostate cancer is the second most diagnosed cancer in men worldwide, following lung cancer [1]. In 2023 alone, the United States saw approximately 300,000 new cases of prostate cancer, resulting in 35,000 deaths [2]. These numbers underscore the urgency to better understand and effectively manage this disease. Not surprisingly, age is a known risk factor, with the median age at diagnosis being 67 years old [2, 3].
Jesse Mack: And as men age, they often contend with many health issues, leading to the concurrent use of multiple medications to manage these conditions—also known as “polypharmacy” [4, 5]. This reliance on multiple medications poses additional challenges, particularly the heightened risk of drug–drug interactions, or DDIs [5]. As such, there’s a critical need to identify and address potential DDIs in these cases.
Judeth Bianco: Drug interactions occur by way of various mechanisms, including both pharmacokinetic and pharmacodynamic interactions [6, 7]. Even though it’s important to consider the molecular and physiological basis for all types of DDIs, today we’ll primarily be focusing on the metabolic and drug-transporter pharmacokinetic interactions—these involve cytochrome P450 enzymes, or CYPs, and P-glycoproteins, or P-gps [6]. CYPs are responsible for metabolizing approximately 75% of drugs in the liver; when activated, the CYP enzymatic activity can be inductive or inhibitory, ultimately altering the plasma drug concentration and potentially modifying efficacy and/or the adverse drug reaction occurrence [6, 8].
Jesse Mack: So, basically an induction of CYP enzymes could increase the metabolism of their substrates, resulting in reduced drug effects, and CYP enzyme inhibition could lead to decreased drug metabolism, which could increase drug concentration and the risk for adverse effects. This applies to drugs that are metabolized by the CYP enzymes [6].
Judeth Bianco: Exactly, and DDIs may also impact the metabolic conversion of prodrugs to their active metabolites by way of CYP enzymes. In the case of a prodrug, CYP induction can increase production and/or concentration of its active metabolite [8]. It’s also possible for coadministered drugs to have DDIs that don’t cause meaningful clinical outcomes; this is observed when a drug is metabolized via several metabolic pathways involving different CYP enzymes and/or P-gp [9]. These scenarios can occur when coadministered drugs have a high therapeutic index, or a wide range of concentrations at which the agent can remain effective without toxic effects [10]. However, the risk of adverse events due to DDI is more pronounced when medications with a narrow therapeutic index, such as warfarin or immunosuppressants (some examples include cyclosporine or sirolimus) are coadministered with strong inducers of CYP enzymes [10].
Jesse Mack: Additionally, it’s worth noting that the activity and expression levels of each CYP can vary significantly among individuals because of genetic differences [11, 12]. For example, gene duplication of CYP2D6, which metabolizes many antidepressants, has been identified as a mechanism of poor response in the treatment of depression [11]. It has also been suggested that patients who carry CYP2C9 polymorphic alleles 2 and 3 are more susceptible to bleeding complications with warfarin treatment [11].
Judeth Bianco: These are all important factors that healthcare professionals should consider when treating patients with different comorbid conditions in order to minimize, if not avoid, the risk of unintended DDIs.
Jesse Mack: Thank you, Judeth. Now let’s delve into enzalutamide, a nonsteroidal androgen receptor pathway inhibitor indicated for the treatment of men with castration-resistant prostate cancer, metastatic castration-sensitive prostate cancer, and non-metastatic castration-sensitive prostate cancer with biochemical recurrence at a high risk for metastasis [6, 13]. Enzalutamide is administered once daily as an oral medication at 160 mg per day [13]. And patients receiving enzalutamide for advanced prostate cancer should be undergoing testosterone suppression with androgen deprivation therapy, either by receiving a gonadotropin-releasing hormone, or GnRH, agonist or antagonist concurrently, or they have had a bilateral orchiectomy [6, 13, 14]. Enzalutamide undergoes hepatic metabolism primarily by CYPs 3A4 and 2C8 to form an active desmethyl metabolite and an inactive carboxylic acid metabolite [6, 10, 15].
Judeth Bianco: Enzalutamide is metabolized by these CYP enzymes. Jesse, could you also describe some of the effects enzalutamide has on a few notable CYPs?
Jesse Mack: Sure, enzalutamide is a moderate inducer of CYPs 2C9 and 2C19, and a strong inducer of CYP3A4 [6, 9, 10]. And because of that, enzalutamide has the potential for DDIs when coadministered with a broad range of drugs that are CYP substrates due to induction of these important enzymes—resulting in possible loss of efficacy or increased risk of drug-related adverse events [6, 9, 13, 16]. The potential impact of enzalutamide on the metabolism and/or bioavailability of other therapeutic agents will be discussed in more detail by our panel experts based on several patient case studies.
Judeth Bianco: It’s no surprise that prostate cancer, particularly in patients over 65 years of age, often coexists with a myriad of comorbidities, including hypertension, high cholesterol, diabetes, cardiovascular diseases, chronic pain, depression, anxiety, and others [6, 17]. As a result, these patients commonly find themselves juggling multiple medications alongside their prostate cancer treatments. With all this in mind, we’d like to discuss the complicated question: How do we navigate these potential interactions to ensure patient safety and treatment efficacy? Let’s talk to the experts and have both Drs. Looney and Morgans walk us through a few hypothetical patient cases to help us understand the potential for drug-drug interactions with enzalutamide and discuss strategies or best practices to minimize the risk. As noted at the beginning, these are fictional cases discussed in the podcast, and they do not represent actual patient cases. And we will start with Dr. Looney—the floor is yours.
Brooke Looney: Thank you, Judeth and Jesse, for this opportunity to be here with Dr. Morgans and share my clinical experience and approach to managing a patient diagnosed with metastatic castration-sensitive prostate cancer, or CSPC. John is 69 years old and has a prior history of cardiovascular disease with a recent episode of deep vein thrombosis, or DVT, in his leg.
Jesse Mack: Now before we discuss John’s treatment, can we talk about the significance of a prostate cancer patient with concurrent cardiovascular disease?
Brooke Looney: Sure. It’s estimated that 30% of patients with prostate cancer have known cardiovascular risk factors such as obesity, diabetes, hypertension, and hyperlipidemia at the time of diagnosis [18]. And 7.5% of males aged 60–79 years old, the group most frequently diagnosed with prostate cancer, have cardiovascular disease [18]. And currently, cardiovascular disease is the leading cause of death in patients with prostate cancer, accounting for approximately 1 in 4 deaths [18].
Jesse Mack: So this really solidifies the importance of being able to manage the drugs used to treat and/or control these comorbidities in elderly patients with prostate cancer. Now back to John, what treatment is he receiving for his prostate cancer?
Brooke Looney: John is prescribed enzalutamide in combination with an oral GnRH antagonist, relugolix, as his treatment for metastatic CSPC. Prostate cancer requires a multi-faceted approach to treatment. And a majority of patients undergo treatment with enzalutamide plus androgen deprivation therapy, or ADT. Injectable ADTs, such as leuprolide, goserelin, triptorelin, and degarelix, aren’t metabolized by hepatic CYPs and are not known to interact with enzalutamide [6, 19]. For convenience, an increasing number of patients are turning to the oral GnRH antagonist, relugolix, which was shown in a clinical trial to be safe and effective when coadministered with enzalutamide with no dose adjustment required—even though relugolix is a substrate of CYP3A, CYP2C8, and P-gp [6, 20, 21].
Jesse Mack: And how is his cardiovascular disease being managed?
Brooke Looney: Given his prior episode of DVT, John is prescribed apixaban, a direct oral anticoagulant, or DOAC.
Judeth Bianco: We know there are some concerns when prescribing enzalutamide with DOACs. Are there any red flags to prescribing enzalutamide and relugolix for use concurrently with apixaban?
Brooke Looney: Yes—apixaban is subject to potential DDIs by dual inhibitors and inducers of CYP3A4 and P-gp [6, 22]. And since enzalutamide is a strong CYP3A4 inducer and a mild P-gp inhibitor, it may result in a decrease in apixaban plasma concentration and exposure [6]. However, the effect of enzalutamide on the plasma concentration of apixaban isn’t very clear because of the opposing CYP3A4 and P-gp interactions.
Judeth Bianco: What’s the best way then to proceed with apixaban or other drugs where the effects of coadministration aren’t clear?
Brooke Looney: Based on the current prescribing information, coadministration of DOACs, including apixaban, with enzalutamide should be carefully monitored with possible changes to dosing to ensure that drug efficacy and safety are maintained [6]. As a standard practice, I would recommend that a thorough patient evaluation be conducted prior to DOAC initiation; this should include assessment of baseline laboratory values, concomitant drug therapies, and comorbidities.
Jesse Mack: Considering the potential risks of drug-drug interactions between enzalutamide and apixaban, are there other alternatives you would recommend for managing John’s DVT? Specifically, would warfarin be a viable option? Given that enzalutamide reduces warfarin’s AUC by 56% and its Cmax by 17%, could this combination still be effective for John [6, 13]?
Brooke Looney: Warfarin is a substrate of CYP2C9 and CYP3A4 and has a narrow therapeutic index [6, 23]. Since enzalutamide is a strong CYP3A4 inducer and a moderate CYP2C9 inducer, it also has the potential to decrease the effect of warfarin by decreasing its exposure. I’d say that coadministration of enzalutamide and warfarin should be avoided if at all possible, or additional INR monitoring should be conducted if coadministration of these two drugs is unavoidable [6]. We still have some other options—there are DOACs that are minimally metabolized by CYP enzymes and are only subject to DDIs with inhibitors and inducers of P-gp [6, 22]. Two examples of these are dabigatran and edoxaban [6, 22].
Jesse Mack: Since these two DOACs are minimally metabolized by CYP enzymes, what does that mean for their interactions with enzalutamide?
Brooke Looney: Well, enzalutamide has been reported to be a mild inhibitor of P-gp [6, 24], so there is potential for a DDI with these DOACs. But there may be less of an interaction than we’d see with apixaban, with the possible exception for patients with renal impairment [6, 25]. Dosing of dabigatran and enzalutamide should be based on the indication and level of renal dysfunction [6, 25]. And I would highly recommend a consult with a pharmacist to assist with the appropriate dose reduction of dabigatran or to determine if another DOAC is warranted.
Jesse Mack: These are great insights—thank you so much Dr. Looney. Now, let’s have Dr. Morgans share a different case of an elderly gentleman undergoing active treatment with enzalutamide for prostate cancer and receiving other medications concomitantly to manage his hypertension and high cholesterol.
Judeth Bianco: Thanks Jesse; let’s start with some basics. Dr. Morgans, could you discuss the prevalence of high cholesterol and hypertension as risk factors for cardiovascular disease in prostate cancer patients?
Alicia Morgans: Of course. Echoing what Dr. Looney mentioned earlier, cardiovascular disease is actually the most common cause of death in prostate cancer patients [18], with hypertension being one of the most common modifiable risk factors of cardiovascular disease [26]. It contributes to increased morbidity and mortality from heart failure, myocardial infarction, or MI, arrhythmias, and stroke [27–29]. Mortality associated with hypertension has been increasing, particularly among older adults [29]. This is the same population associated with higher overall incidence of malignancy and prostate cancer [29]. In this patient population, it’s important to ensure adequate screening and treatment of high blood pressure, which can manifest for the first time, or worsen, as a result of cancer-directed therapy [29].
Judeth Bianco: Thank you for that explanation; now let’s dig into your patient case.
Alicia Morgans: Bob is a 71-year-old man diagnosed with high-risk, biochemical recurrent nonmetastatic prostate cancer. He has a long history of poorly controlled hypertension and high cholesterol, which would put him at very high risk for cardiovascular disease. Currently, he’s on enzalutamide for his prostate cancer, verapamil for hypertension, and atorvastatin to reduce his elevated cholesterol.
Jesse Mack: For a patient like Bob, could you discuss the potential for drug-drug interactions between enzalutamide and medications like statins or calcium channel blockers?
Alicia Morgans: Of course. Enzalutamide is a strong CYP3A4 inducer, which can potentially reduce atorvastatin exposure, since atorvastatin is a substrate of CYP3A4 and the transporters P-gp and BCRP [6]. So, liver function and lipid levels should be carefully monitored when statins are coadministered with enzalutamide to assess their safety and efficacy.
Jesse Mack: And what would be your approach to monitor lipid levels in a patient receiving a statin alongside enzalutamide?
Alicia Morgans: I would coordinate with the patient’s primary care physician or cardiologist to have them check a patient’s lipid panel before starting statin therapy, and every 6–8 weeks to assess the treatment response [6, 30]. I’d also consider working with those teams to adjust statin dosage levels during therapy if needed [6, 30]. It’s worth noting, though, that the atorvastatin prescribing information does not provide dose adjustment recommendations. If lipid control is satisfactory with no evidence of adverse events, subsequent lipid monitoring can be done every 4–6 months [6, 30].
Judeth Bianco: So, Dr. Morgans, what alternative would you take to manage Bob’s high cholesterol?
Alicia Morgans: Other types of statins, such as pitavastatin, pravastatin, or rosuvastatin, may be suitable alternatives for prostate cancer patients who take enzalutamide, as these agents are minimally metabolized by CYPs and have no known basis for interactions with enzalutamide [6, 31].
Jesse Mack: And now how about the hypertensive agent that Bob was taking? I would think that there might be the potential for drug interactions with calcium channel blockers since these agents are metabolized by CYP3A4.
Alicia Morgans: That’s correct. Most of the commercially available calcium channel blockers are metabolized by CYP3A4, and so there’s potential for a DDI, where enzalutamide may decrease the plasma concentrations of these drugs [6, 10, 13, 32]. If coadministration is necessary, the pharmacologic response of the calcium channel blocker should be monitored closely following the initiation or discontinuation of enzalutamide, and its dosage adjusted as necessary [6].
Judeth Bianco: So, what are the alternative treatment options for managing hypertension for Bob?
Alicia Morgans: One option to consider is using angiotensin-converting enzymes, or ACE inhibitors, like benazepril, which has no known interactions with enzalutamide [6, 33, 34]. Another option could be beta blockers, such as carvedilol, which also have a more favorable interaction profile with enzalutamide [6, 34, 35].
Jesse Mack: This is very useful information. Thank you, Dr. Morgans, for sharing your expertise and insights.
Alicia Morgans: My pleasure. And one final thought—as a medical oncologist for somebody like Bob, I’m always focused on managing and treating his prostate cancer. Rather than making changes on my own to a patient’s blood pressure or cholesterol management plans, I work closely with a pharmacist and primary care and cardiology teams and defer to their clinical expertise in managing Bob’s comorbidities. By working together as a multidisciplinary team, we can successfully optimize long-term outcomes for him.
Judeth Bianco: That’s really great Dr. Morgans, thanks again. Now let’s talk about managing a diabetes patient who is diagnosed with castrate-resistant prostate cancer and start by discussing the prevalence of diabetes among prostate cancer patients. Dr. Looney, could you shed some light on this?
Brooke Looney: Diabetes is highly prevalent among patients with prostate cancer, especially those over the age of 65 [6, 36]. It’s a significant concern that requires careful management alongside cancer treatment. Type 2 diabetes mellitus is the predominant form of diabetes, accounting for about 90% of cases [37]. Type 2 diabetes has been associated with an increased risk of developing several cancers, including liver, pancreatic, colorectal, renal, bladder, endometrial, and breast [37]. Interestingly, several meta-analyses have shown that type 2 diabetes is correlated with reduced risk of prostate cancer [37]. Despite this reduction, diabetes is associated with increased prostate cancer mortality [37]. Available reports and meta-analyses demonstrate that most anti-diabetic drugs do not increase the risk of prostate cancer incidence or disease progression [37]. In fact, some studies have shown a potential advantage of type 2 diabetes mellitus treatment in prostate cancer risk reduction and improvement in patient overall survival associated with metformin therapy [37].
Judeth Bianco: Can you discuss how you would treat a patient with prostate cancer and type 2 diabetes?
Brooke Looney: Here, we have Tim, a 59-year-old male being treated with enzalutamide for castration-resistant prostate cancer. He’s been diagnosed with type 2 diabetes for about 4 years and was prescribed glimepiride.
Jesse Mack: Glimepiride is metabolized in the liver by the cytochrome P450 system. Enzalutamide is a known inducer of both CYP2C9 and CYP3A4, which may contribute to relevant pharmacokinetic interactions between the two drugs [6, 13]. What potential considerations should be taken into account when prescribing enzalutamide alongside glimepiride?
Brooke Looney: Sulfonylureas, including glimepiride and few others within this class of hypoglycemic agents, are primarily metabolized by CYP2C9 [6, 38]. So, there’s the potential for a DDI resulting in reduced plasma concentration of glimepiride when given concurrently with enzalutamide [6]. Use of other antidiabetic agents, such as DPP4 inhibitors, may pose a similar risk, since they are primarily metabolized by CYPs 3A4 and 5 [6, 39]. Because of the potential for these DDIs, we would strongly advise patients like Tim to work with their primary care physician or endocrinologist to carefully monitor their A1C status when taking enzalutamide concomitant with glimepiride, as well as when enzalutamide is stopped. Close monitoring is crucial to ensure that patients like Tim receive safe and effective treatment. And healthcare providers should closely monitor blood glucose levels and adjust medication doses as necessary to optimize diabetes management while minimizing the risk of adverse effects, especially when patients with prostate cancer are taking enzalutamide.
Judeth Bianco: Are there alternative anti-diabetics for Tim that might help reduce the risk of DDIs with enzalutamide?
Brooke Looney: Yes, one possible alternative is metformin, a widely prescribed medication for type 2 diabetes with no known interactions with enzalutamide [6, 40]. SGLT2 inhibitors are also effective in treating type 2 diabetes; importantly, they are not metabolized by CYPs and have no known interactions with enzalutamide. Assuming no contraindications or issues with tolerability, metformin or SGLT2 inhibitors could be safely used with enzalutamide in Tim’s case.
Jesse Mack: These are wonderful insights. Thank you both Dr. Looney and Dr. Morgans.
Judeth Bianco: And we’re almost up to the end of our podcast for today. Before we wrap up, I’d like to ask both panel members to share their final thoughts or key takeaways on this important topic.
Alicia Morgans: Thanks, Judeth. There are a few takeaways I’d like to leave with the listeners: first and foremost, enzalutamide is a beneficial drug for the treatment of certain types of prostate cancer but requires management of potentially significant drug interactions. Most drug interactions stem from the fact that enzalutamide is a strong inducer of CYP3A4, a hepatic cytochrome P450 enzyme that is responsible for the metabolism of many other drugs on the market. Based on the current understanding of enzalutamide drug interactions, nearly all of them can be effectively managed with appropriate knowledge of which drugs pose interaction risks, when dose adjustments are indicated, and when alternative drugs can be substituted [6].
Brooke Looney: I completely agree. And I do have a few additional takeaways for the listeners: where DDIs pose challenges with enzalutamide, it may be possible to alter dosing or prescribe alternative drugs, particularly with the integrated expertise of a multidisciplinary care team [6]. Prescribers should refer to prescribing information to assess the need for medication dose adjustments based on potential CYP or transporter effects. However, it is crucial to recognize that prescribing information may not always capture all possible drug interactions, especially with newer medications [6]. It’s critical that we, as healthcare professionals, keep an open dialogue with our prostate cancer patients and be vigilant of potential polypharmacy throughout their treatment course. And that’s why collaboration among multidisciplinary teams of physicians, pharmacists, and other healthcare practitioners is vital. By pooling our expertise and resources, we can optimize treatment decisions, mitigate risk, and improve patient outcomes.
Judeth Bianco: Thank you both. We also want our listeners to know that we collaborated with other investigators on a recent publication in Drug Safety 2024 entitled “Enzalutamide: Understanding and Managing Drug-Drug Interactions to Improve Patient Safety and Drug Efficacy,” which is a helpful resource with additional information on enzalutamide and related DDIs and a great supplement to this podcast. That’s all we have for today. Have a great day, everyone. Bye.
Declarations
Funding
Funding was provided by Pfizer Inc. and Astellas Pharma Inc.
Conflicts of Interest
All authors have fully considered the Conflicts of Interest policy set forth by the journal. Alicia Morgans has received consulting fees from Astellas Pharma Inc., AAA Pharma Inc., AstraZeneca Pharma LP, Bayer HealthCare Pharma LLC, Curium, Janssen Pharma LLC, Exelixis Inc., Macrogenics, Myovant Sciences, Inc., Merck & Co. Inc., Novartis AG, Lantheus, Telix Pharma Limited, Sanofi S.A., and Pfizer Inc., research fees from Astellas, Bayer HealthCare Pharma LLC, Myovant Sciences Inc., and Pfizer Inc. Brooke Looney receives research support from AstraZeneca Inc. and Pfizer Inc. and has served as a speaker for AstraZeneca Inc. Jesse Mack is an employee of Astellas Pharma Inc. and was a consultant for Pfizer prior to joining Astellas Pharma Inc. Judeth Bianco is an employee of Pfizer Inc.
Ethics Approval
This article does not contain any studies with human participants or animals by any of the authors.
Consent to Participate
Not applicable, as this article does not contain any studies with human participants by any of the authors.
Consent for Publication
All co-authors are aware of the submission to this journal, and agree to allow the corresponding author to serve as the primary correspondent with the editorial office and to review and sign off on the final proofs for publication.
Data Availability
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
Code Availability
Code availability is not applicable as no software application or custom code was used, generated, or analyzed during the current study.
Author Contributions
All authors have contributed equally to the manuscript development (i.e., concept and planning of the work described; acquisition, analysis and interpretation of the data; critical review and revision of the manuscript; and approved the final submitted version of the manuscript). All authors read and approved the final version.
Medical Writing, Editorial, and Other Assistance
Editorial support for this podcast was provided by Jack Liao, PhD, at Impact Communication Partners.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
