Table 1.
Properties of approved therapies and therapies in clinical trials on Lp(a) plasma levels
Name | Drug type | Drug target | Route of administration | Dosing frequency | Phase | Effect on Lp(a) levels |
Statins | Competitive inhibitor | HMGCR | Oral | Daily | Approved | +10 to 20% (varying by type of statin) [19] |
Ezetimibe | Cholesterol absorption inhibitor | NPC1L1 | Oral | Daily | Approved | No effect [20] |
Lipid apheresis | Apheresis | NA | NA | Weekly | Approved in USA | –63% postapheresis [26] |
PCSK9i antibodies | Monoclonal antibody | PCSK9 | Subcutaneous | Every 2 weeks | Approved | –27% [21,22] |
Inclisiran | Small interfering RNA | PCSK9 | Subcutaneous | Twice yearly | Approved | –19% to –26% [35] |
Pelacarsen | GalNAc-conjugated antisense oligonucleotide | LPA mRNA | Subcutaneous | Once monthly | Phase 3 | –80% [29▪▪] |
Olpasiran | GalNAc-conjugated siRNA | LPA mRNA | Subcutaneous | Every 3 months | Phase 2 | Up to –90% [31▪] |
GalNAc, N-acetylgalactosamine; HMGCR, 3-hydroxy-3-methylglutaryl coenzyme reductase; Lp(a), lipoprotein(a); NPC1L1, Niemann-Pick-like protein 1C1; PCSK9i, proprotein convertase subtilisin kexin type 9 inhibiting; siRNA, small interfering RNA.