The Drugs That Finally Lower Lp(a): What's Coming and When We'll Know If It Saves Lives
There is one number I test in my patients that, until recently, I could explain but not treat. It is called lipoprotein(a), usually written Lp(a) and said out loud as “L-P-little-a.” It is an inherited form of cholesterol particle, and when it runs high it pushes up the risk of heart attack, stroke, and a narrowing of the heart’s main valve. For years I have been in the strange position of telling patients their Lp(a) is elevated, that it matters, and that there is no drug aimed directly at it. We lower everything around it instead and hope to offset the risk.
That era is ending. Several medicines now in late-stage testing can cut Lp(a) by around 90 percent, a degree of lowering we have never had. The honest catch, and the reason I am writing this as a preview rather than a prescription, is that we do not yet know whether driving the number down actually prevents heart attacks. The trials that will answer that are reading out over the next year or two. Let me explain what is coming and why I am both excited and patient about it.
A quick reminder of why Lp(a) is different
Most of the cholesterol problems I treat respond to the tools we have. LDL cholesterol comes down with statins, with PCSK9 inhibitors, and with diet. Lp(a) is stubborn in a way those do not prepare you for. It is set almost entirely by the genes you inherited, it barely moves with diet or exercise, and the usual cholesterol drugs do little to it. About one in five people worldwide has a high level, most of them have no idea, and it travels in families. I cover the full background in my guide to lipoprotein(a) and wrote recently about new data on very high Lp(a) levels above 175.
Because nothing targeted it, my whole strategy for a patient with high Lp(a) has been indirect. Drive the LDL as low as possible, control blood pressure, address every other risk factor hard, and use tools like a coronary calcium score to gauge how much disease has already built up. That approach helps. It just never addressed the Lp(a) itself.
The new drugs and how they work
The medicines in development take a clever approach. Instead of trying to clear Lp(a) out of the blood, they go upstream and tell the liver to make far less of it in the first place. They do this by interfering with the genetic instructions the liver uses to build the particle. You do not need the molecular details to get the point. These drugs quietly turn down production at the source.
Several are in the running. Most are injections given somewhere between monthly and a few times a year, and in their earlier studies they reduced Lp(a) by roughly 80 to 90 percent or more, which is dramatic. One of them is a pill taken daily, which would be even easier if it pans out. The companies behind them are the same major players developing the rest of the modern cholesterol toolkit, so there is serious effort and money behind getting these across the line.
What strikes me is how cleanly they work on the number. We have never been able to move Lp(a) like this. For a patient who has watched an unfavorable inherited number sit on their lab report for years with nothing to do about it, the idea that we can now cut it by ninety percent is genuinely new.
The question that actually matters
Here is where I slow patients down, because the excitement can run ahead of the evidence. Lowering a number is not the same as preventing an event. We believe high Lp(a) causes heart disease, based on strong genetic and population data. The logical next step is that lowering it should reduce heart attacks and strokes. Logical is not the same as proven.
The history of cardiology is full of treatments that improved a lab value and then failed to help patients, or even hurt them, when they were finally tested in a proper trial. That is why we run large studies that track real events, not just lab numbers. For these Lp(a) drugs, those studies are underway right now. They have enrolled many thousands of people with high Lp(a) and existing heart disease or high risk, given them either the drug or a placebo, and they are waiting to count heart attacks, strokes, and cardiovascular deaths in each group.
The first of these big outcome trials are expected to report results around the end of 2026 and into 2027. When they do, we will finally know whether lowering Lp(a) delivers what the biology promises. If the answer is yes, it will be one of the most important advances in preventive cardiology in a generation, because it closes a gap we have never been able to close. If the answer is disappointing, it will be a hard but valuable lesson, and far better to learn it from a trial than from treating patients on a hunch.
What this means for you right now
If your Lp(a) is high, the practical advice today has not changed, and I do not want the headlines about future drugs to distract from it. The proven move is to attack everything we can already treat. Get your LDL as low as your risk warrants, because lifetime LDL exposure tracks directly with the risk of dying from heart disease and lowering it hard is something we know works. Control your blood pressure. Do not smoke. Consider a coronary calcium score to see how much disease is actually present. These steps reduce your overall risk regardless of what your Lp(a) does, and they are available now rather than in a year.
It is also worth knowing your number if you have never been tested, and worth having your first-degree relatives tested if yours is high, because Lp(a) runs in families and a high level often flags several people in a household who do not know they are at risk. You only need the test once in your life, since the level is largely fixed by your genes.
When the new drugs arrive, assuming the trials are positive, the people most likely to benefit are exactly those with high Lp(a) who remain at high risk despite doing everything else right. That is the group I think about most, the patients who have lowered their LDL, controlled their pressure, and still carry an inherited risk we could not touch. For them, a drug that finally addresses the Lp(a) itself would be a real addition.
My take
This is the development I am watching most closely in my own field. For the first time we can lower Lp(a) dramatically, and within a year or two we should know whether that lowering prevents the events we have always feared it causes. I am optimistic, because the genetic evidence pointing to Lp(a) as a true cause is about as strong as this kind of evidence gets. I am also disciplined about it, because optimism is not proof, and my job is to recommend what the trials show rather than what I hope they will show. If you have high Lp(a), the smartest thing you can do today is treat everything else relentlessly and stay tuned. The answer to the question we have been asking for decades is finally coming.
Frequently Asked Questions
What is lipoprotein(a)?
Lipoprotein(a), or Lp(a), is an inherited type of cholesterol particle in your blood. When it is high, it raises the risk of heart attack, stroke, and narrowing of the heart’s aortic valve. Your level is set mostly by your genes, it barely changes with diet or exercise, and about one in five people has a high level, usually without knowing it.
Why can’t statins lower Lp(a)?
Statins are excellent at lowering LDL cholesterol but have little effect on Lp(a), because Lp(a) is produced and regulated differently and is driven largely by genetics. Diet and exercise also do little to it. This is why Lp(a) has been so frustrating to treat and why a targeted drug would be such a meaningful addition.
What are the new Lp(a)-lowering drugs?
They are medicines, mostly injections given between monthly and a few times a year, with one daily pill in development, that reduce how much Lp(a) the liver makes. In earlier studies they lowered Lp(a) by roughly 80 to 90 percent or more, a level of reduction no existing treatment achieves. Several are now in large trials run by major pharmaceutical companies.
When will we know if they work, and when can I get one?
The large trials testing whether lowering Lp(a) actually prevents heart attacks and strokes are expected to report results around late 2026 into 2027. None of these drugs is approved for general use yet. Approval and availability will depend on those trial results and FDA review.
What should I do now if my Lp(a) is high?
Focus on what we can already treat. Lower your LDL cholesterol as much as your risk warrants, control your blood pressure, do not smoke, and consider a coronary calcium score to see how much plaque is present. These steps lower your overall risk regardless of your Lp(a). Also have your first-degree relatives tested, since high Lp(a) runs in families.
References
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Tsimikas S, Karwatowska-Prokopczuk E, Gouni-Berthold I, et al. “Lipoprotein(a) Reduction in Persons with Cardiovascular Disease.” New England Journal of Medicine 382, no. 3 (2020): 244-255.
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O’Donoghue ML, Rosenson RS, López JAG, et al. “Olpasiran for Lowering Lipoprotein(a) (OCEAN(a)-DOSE).” New England Journal of Medicine 387, no. 20 (2022): 1855-1864.
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Nissen SE, Wang Q, Nicholls SJ, et al. “Lepodisiran, an Extended-Duration Short Interfering RNA Targeting Lipoprotein(a).” JAMA, 2025.
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Family Heart Foundation. “Ongoing Clinical Trials Targeting Lipoprotein(a).” Accessed 2026.
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Reyes-Soffer G, Ginsberg HN, Berglund L, et al. “Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association.” Arteriosclerosis, Thrombosis, and Vascular Biology 42, no. 1 (2022): e48-e60.
Published on damianrasch.com. The above information was composed by Dr. Damian Rasch, drawing on individual insight and bolstered by digital research and writing assistance. The information is for educational purposes only and does not constitute medical advice.