1609 studies (119 landmark), 10 trials tracked, 10 guideline documents, 12 Radcliffe videos. Updated 18 August 2026.
| Trial | Agent | N | Status | Registry |
|---|---|---|---|---|
| Lp(a)HORIZON | Pelacarsen | 8,323 | Completed, results awaited | |
| OCEAN(a)-Outcomes | Olpasiran | 7,297 | Ongoing, primary completion March 2028 | |
| ACCLAIM-Lp(a) | Lepodisiran | 17,300 | Ongoing, enrolment complete, primary completion March 2029 | |
| MOVE-Lp(a) (muvalaplin outcomes) | Muvalaplin | 10,450 | Recruiting, primary completion March 2031 |
All 10 trials in the tracker · The agents
RNA therapeutics
Review of the Lp(a)-lowering pipeline through mid-2026, covering trial data, regulatory updates and registries. Five agents across three mechanisms have reached late-stage development. Pelacarsen, a GalNAc-conjugated antisense oligonucleotide, lowers Lp(a)…
PCSK9 inhibition
In the CAVIAR trial, heart transplant recipients treated with the PCSK9 inhibitor alirocumab showed slower progression of cardiac allograft vasculopathy (CAV), but only among those with concomitantly elevated LDL-C and lipoprotein(a). The authors frame this…
Testing
Review of lipoprotein(a) in premature atherosclerotic cardiovascular disease (ASCVD), defined as an event before age 55 in men or 65 in women. Elevated Lp(a) is an independent, causal, genetic risk factor linked to progression of high-risk coronary plaques,…
Epidemiology
Secondary analysis of the Multi-Ethnic Study of Atherosclerosis (MESA), examining how metabolic dysfunction-associated steatotic liver disease (MASLD, defined by CT liver attenuation) relates to lipoprotein(a) and long-term outcomes. Median Lp(a) was lower…
Every adult, at least once in a lifetime: that is the recommendation of the 2019 ESC/EAS guidelines, the 2022 EAS consensus statement, the 2021 Canadian guidelines, the 2024 NLA update and the 2026 ACC/AHA multisociety guideline. Because plasma Lp(a) is more than 90 percent genetically determined and stable over decades, one measurement usually settles it; repeat only when a value sits close to a decision threshold, after menopause, in kidney disease, or when a new therapy is started. Cascade testing of first-degree relatives is recommended when the index value is high.
Prefer nmol/L on an isoform-insensitive assay: it counts particles, and apo(a) size varies so much between people that mass units mislead. Conversion is only approximate; a flat factor of 2.0 to 2.5 misclassifies about one in ten patients around trial thresholds, and the Copenhagen conversion formula does better (Lp(a)HORIZON screening data, 2026). Quote whatever unit the laboratory reported and do not convert for a decision if you can re-measure instead.
Risk is continuous. Common markers: below 30 mg/dL (75 nmol/L) low; 50 mg/dL (125 nmol/L) the traditional risk-enhancer threshold used by most guidelines; 70 mg/dL (about 150 nmol/L) the Lp(a)HORIZON entry level; 90 mg/dL and 175 to 200 nmol/L the entry levels of the other outcomes trials; above 180 mg/dL (about 430 nmol/L) a lifetime risk equivalent to heterozygous FH. About one in five adults is above 50 mg/dL; distributions differ by ancestry, the risk per nmol/L largely does not.
Statins do not (they raise it 8 to 20 percent), nor do ezetimibe, bempedoic acid, fibrates or omega-3 fatty acids. PCSK9 monoclonal antibodies lower it 20 to 30 percent and inclisiran about 22 percent; CETP inhibition (obicetrapib) about 37 percent; niacin about 37 percent but without outcome benefit; lipoprotein apheresis 60 to 70 percent per session. None of these is an Lp(a) therapy. What works today is intensive control of everything else, LDL-C first, because Lp(a) and LDL-C risk are independent and additive.