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Amgen olpasiran may fill critical treatment gap in lowering Lp(a): GlobalData

The latest data from the final analysis of the Phase II OCEAN(a)-DOSE study showed that olpasiran reduced Lp(a) levels in patients by 95 per cent

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Amgen’s olpasiran, a small interfering RNA (siRNA), is making strides in reducing Lp(a) levels significantly in patients with cardiovascular disease. This is noteworthy as elevated Lp(a) is considered a potent risk factor for heart disease and stroke. It also underscores olpasiran’s potential to address a vital treatment gap, representing a pivotal advancement in the realm of dyslipidemia, according to GlobalData.

The latest data from the final analysis of the Phase II OCEAN(a)-DOSE study showed that olpasiran reduced Lp(a) levels in patients by 95 per cent. This study, which resulted from the off-treatment extension period, showed that patients taking 75 mg of Olpasiran previously every 12 weeks presented a 40–50 per cent reduction in LP(a) for nearly a year after their last dose.

Lp(a) is an atherogenic particle and an independent predictor of CV risk. Elevated levels of Lp(a) in the blood are considered a risk factor for CVD, including heart attack and stroke, as it promotes the formation of blood clots and plaque buildup in the arteries. There are a few strategies that have been shown to lower Lp(a) levels, including niacin, Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, antisense oligonucleotides, and lifestyle modifications. GlobalData forecasts olpasiran sales to reach $1.05 billion in 2029.

Dr Shireen Mohammad, Cardiovascular and Metabolic Disorders Analyst at GlobalData, comments, “At present, there are no specific therapies available in the market that target Lp(a) directly. The standard treatments for dyslipidemia, such as statins and other cholesterol-lowering drugs, are not effective in reducing Lp(a) levels. Therefore, there is a high level of unmet need for therapies targeting other lipid particles, particularly the Lp(a) particle.

Olpasiran is a promising drug treatment for dyslipidemia as it works by preventing the assembly of Lp(a) and therefore the translation of the apo(a) protein, hence reducing Lp(a) in the circulation. Amgen is currently enrolling patients for a Phase III study.”

 

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