Combination Therapeutics & Innovations to Sustain Pulmonary Arterial Hypertension Treatment Market

Owing to non-responsive nature of several advance pharmacotherapies and high diagnosis and treatment costs, researchers and medical practitioners in the global pulmonary arterial hypertension treatment market are continually working on favorable and effective alternative treatment models and increase survival rate among the patients with pulmonary arterial hypertension.

Future Market Insights, in its recently published outlook on the global market for pulmonary arterial hypertension treatment market, projects the US$ 5 billion market to barely exceed US$ 6.5 billion in terms of revenue, through the next decade. The market has been estimated at a sluggish CAGR of 2.5% over 2018-2028. However, innovations and combination therapeutics are likely to forestall further decline of the pulmonary arterial hypertension treatment market in near future.

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Cancer Protein Molecules Tested for Potential Therapeutic Use- to Prevent Pulmonary Arteries ‘Scarring’

Scarring or Fibrosis, in pulmonary arterial hypertension, is an important cause of damage to pulmonary arteries, which in turn, strains the heart functions- eventually leading to breathlessness. Recently, researchers from Brigham and Women's Hospital conducted a study using network medicine- a method of establishing correlation between proteins, pathways and more- and identified the cancer protein NEDD9 and its molecular mechanisms as a potential treatment for PAH patients. The study has identified that a specific amino acid residue in the cancer protein is expected to play a crucial role in controlling and regulating the severe consequences of scarring.

BH4- Factor Controlling Production of Nitric Oxide- Shows Promising Result on Rat Model; Results Show Lower Lung Hypertension

Researchers at Imperial College London and Bar-Ilan University, Israel explored the properties of naturally occurring tetrahydrobiopterin (BH4) and its subsequent role in effective treatment for lung hypertension and right heart failure. BH4 controls the production of endothelial nitric oxide synthase (eNOS) in the human body. eNOS produces nitric oxide which is important for healthy endothelial cells- forming the inside lining of blood vessels. Nitric oxide is responsible for dilating blood vessels, working to lower lung blood pressure.

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The study- conducted on a rats first in injected with chemical triggering pulmonary hypertension and then an injection of BH4, showed signs of decreased lung pressure, stronger heart contractions and, enlarged heart. The rats were then given BH4 in food before the chemical that previously induced pulmonary hypertension. As a result of which, no thick layers of smooth muscles were developed- often leading to lung hypertension.

After the phase 1 of clinical trials, the patients- administered BH4 orally, showed improved exercise capacity- an indicator of low pressure in lungs. It is anticipated that BH4, when given controlled measure could prove to a valuable treatment for pulmonary arterial hypertension patients who otherwise are not responsive to regular medication.

With Treatment Options, ‘Accurate Risk Measuring’ Tools is the Need of the Hour

Although measurable efforts are being made in the global pulmonary arterial hypertension treatment market, the survival rate among PAH patients continues to remain low. According to studies, the average life expectancy of PAH patient is approximately 3 years from symptom onset- being at a risk of disease progression and frequent hospitalizations. Several studies indicate that early diagnosed and ‘low-risk’ patients stand a chance of improved survival if the risk is calculated accurately. Experts have expressed the need to develop appropriate and accurate risk prediction tools improve treatment outcomes in PAH patients.

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Increasing prevalence and incidence rate is driving the global pulmonary arterial hypertension treatment market. Advancements are being made for early diagnosis and improved treatment.

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This release was published on openPR.