Opinion

The New Medical Frontier: Understanding the Mechanism of Disease for Better Care

The high cost of health care is not a new discussion. Each day, we are inundated with heartbreaking stories of patients without access to essential therapies due to rising costs or the inability to pay momentous medical bills.

As a public, it is clear we recognize this challenge; however, despite years of discussion, we have not yet been able to create a workable solution that lowers the cost of care, increases access and ultimately gives patients better outcomes.

Perhaps part of the challenge is that we are seeking a silver bullet solution — a one-stop policy answer that will cost less, bring a better quality of life and fix an inherently broken system. To date, plans have focused on shifting cost structures or establishing better regulation, attempting quick, far-reaching solutions to a complex problem. This doesn’t work.

The challenge is that our system of health care is not situated for such easy solutions. The United States health care system is complicated with layers of regulation and a vast number of stakeholders, including providers of treatments, governmental overseers and those within the distribution channels.

Each of these stakeholders influence the ultimate consumer (or victim) of the chain: the patient. To be most effective, a solution must ensure that all stakeholders — payers, technology developers, regulators, doctors and patients — take some level of responsibility to address these challenges.

Viewing this through the lens of drug development provides an understanding of this challenge, showing where greater stakeholder involvement can lead to better access. Consider the context of moving products through research and development, especially within regulatory systems that are conveniently grouped into organ systems — e.g. cardiology, neurology, dermatology, rheumatology, etc.

Historically, the grouping system created a framework for easy categorical organization. It reduces products to the most simplistic nature to streamline the regulatory process.

Today, however, we are realizing this grouping has become inadequate at best and does not represent the mechanisms of disease at their very base. Take, for example, cardiovascular disease.

We now know that several factors can contribute to an individual patient’s diagnosis of cardiovascular disease. Further, those underlying conditions can mean that a treatment protocol that works for one patient will not only fail for another but may cause another debilitating disease. There is a myriad of challenges, especially when regulatory systems cannot keep up with science, increasing time and overall costs of product development, which both increase product price and withhold important therapies from patients who require them most.

There is, however, a ray of hope: In the area of cancer molecular therapy, agencies such as the Food and Drug Administration have finally begun to appreciate the mechanistic aspects of cancer development, and thus, products that address these specifically. Entrectinib was recently approved for NTRK gene fusion positive solid tumors, a key step in the direction of evaluating the correlative molecular signature and a drug that could alter such signaling agnostic to a specific tumor type (although this approval was also part of the approval for ROS1-positive non-small cell lung cancer, as well).

We need these types of efforts to continue. Today, we know that rheumatologic diseases, such as rheumatoid arthritis, lupus, psoriasis and other such diseases where the body is attacked by one’s own immune system, are thought to be caused and aggravated by inflammation. We also know that these diseases are highly associated with cardiovascular diseases like atherosclerosis.

In patients with rheumatologic diseases, such atherosclerosis is accelerated; the presence and progression are higher and faster than patients without such diseases. Patients with rheumatoid arthritis have a 50 percent higher chance of dying of a heart attack; cardiovascular disease is the leading cause of death in lupus patients, accounting for one-third of all deaths in patients harboring this diagnosis.

Yet, despite evidence suggesting anti-inflammatory approaches may protect patients an additional 15 percent above use of drugs such as statins, there are no recommendations from preventative medicine task forces or scientific groups to primarily address this area of risk for patients. Moreover, this has not been an area where expertise within inflammation, overlapping traditional therapeutic areas such as cardiology and rheumatology, exist within regulatory bodies. This creates significant issues within the entire value chain, decreasing efficiency in therapeutics development, and ultimately, the health of afflicted patients.

Today, our call to action is mechanistic. It is understanding that — from recommendations of therapeutic societies to assessment of the safety and efficacy of given therapeutics and even to our continuing education efforts — we must assess the new frontier of the overlap between the traditional therapeutic areas. Our charge is to see and really understand what is actually happening to our patients and what is manifest across organ systems.

We must understand biology extends past the convenience of traditional disciplines in medicine and encompasses a widening therapeutic population, in whatever part of the value chain we play a role. Using this lens, we can create solutions to diseases that are smarter, more efficacious and more cost effective, for the benefit of the patient.

 

Bert Liang is CEO of Abcentra, which is developing a pipeline of therapeutic monoclonal antibodies for serious inflammatory diseases where medical treatments are either not available or better options are needed.

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