Lp(a) in Atherosclerotic cardiovascular disease
- Primary identifiers
- 9
- Sponsors tracked
- 6
- Evidence types
- 2 of 3
- Last refreshed
- 2026-07-28 · daily
MightyRayn panel synthesis
OmniRayn’s reading of this landscape — our interpretation, not a registry fact
The largest bet in cardiovascular medicine currently resting on no outcome data at all. Lp(a) is an inherited, causal risk factor on genetic evidence, and these agents cut circulating levels by roughly 80 to 90 percent — but as of the reviews cited here, no therapy has been approved that specifically lowers Lp(a), and none has shown a reduction in cardiovascular events. The registry shows three outcome trials each enrolling on the order of ten thousand participants, which is the industry committing at enormous scale to a biomarker whose translation is modelled rather than demonstrated. Two things to watch. Modelling implies a large ABSOLUTE reduction is what matters, so percentage lowering may be the wrong yardstick and a patient's starting level may decide who benefits. And route is already separating the field: injectable antisense and siRNA agents dominate, while oral small molecules that block particle assembly have now reached Phase 3 — a materially different adherence profile for a lifelong preventive indication.
Programs and primary evidence
| Sponsor | Asset | Phase | Mechanism | Primary source |
|---|---|---|---|---|
| Amgen | Olpasiran (OCEAN(a) Outcomes) | 3 | siRNA against apolipoprotein(a) synthesis |
|
| Amgen | Olpasiran (primary prevention) | 3 | siRNA against apolipoprotein(a), moved to primary prevention |
|
| Amgen | Olpasiran (plaque imaging) | 3 | imaging endpoint rather than an event endpoint |
|
| Novartis Pharmaceuticals | Pelacarsen with background inclisiran | 3 | antisense oligonucleotide against apo(a), on top of an LDL-lowering siRNA |
|
| Eli Lilly and Company | Muvalaplin (oral) | 3 | oral small molecule blocking Lp(a) particle formation |
|
| Novartis Pharmaceuticals | DII235 | 2 | second Lp(a)-lowering agent from the same sponsor |
|
| Shenzhen Salubris Pharmaceuticals | SAL0137 (oral) | 2 | oral agent for elevated Lp(a) |
|
| Qassim University | review | — | apo(a) synthesis inhibition and particle-assembly inhibition |
|
| International Hellenic University | review | — | GalNAc-conjugated ASO and siRNA hepatocyte targeting; oral inhibitor of particle formation |
|
Method and limits
- Programs are enumerated from primary registries (ClinicalTrials.gov, PubMed). A program appears here only if a primary record links this target to this indication as a therapeutic hypothesis — associations and risk markers are excluded by design.
- Every claim above carries the identifier it rests on. We report what the record states; we do not assert efficacy, and computational findings are pending wet-lab confirmation.
- Absence is not evidence of absence: unregistered, non-US and stealth-stage programs are not visible to these sources.
- This page refreshes daily (new primary entity 1d ago — landscape still moving). Mechanism classifications are our reading of the public record and may be revised.
Want the analysis behind this landscape?
The public page is the map. The full dossier adds differentiation analysis, kill-tests and the whitespace read for this target — the parts we do not publish.