Safety and Efficacy of Novel Agents: Pelacarsen, Obicetrapib, and Beyond

Priya Palimkar; Priyanka Satish; Rakendu Jayasree Rajendran; Hema Malathi Rath; Rajni Sharma

doi:10.25259/IJCDW_66_2025

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Review Article

Cardiovascular

10 (

); 334-339

doi:

10.25259/IJCDW_66_2025

Safety and Efficacy of Novel Agents: Pelacarsen, Obicetrapib, and Beyond

Priya Palimkar^1,, Priyanka Satish², Rakendu Jayasree Rajendran³, Hema Malathi Rath⁴, Rajni Sharma⁵

1Department of Cardiology, Sahyadri Hospital, Pune, Maharashtra, India,

2Department of Cardiovascular Prevention, Ascension Texas Cardiovascular, UT Dell Medical School, Austin, Texas, United States

3Department of Internal Medicine, Virtua Health, New Jersey, United States,

4Department of Cardiology, The Heart Care Clinic, Kolkata, West Bengal, India.

5Department of Cardiology, Max Super Speciality Hospital, New Delhi, India.

*Corresponding author: Priya Palimkar, Department of Cardiology, Sahyadri Hospital, Pune, Maharashtra, India. drpriyapalimkar@gmail.com

Received: 2025-10-08, Accepted: 2025-11-25, Epub ahead of print: 2025-12-20, Published: 2025-12-27

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Palimkar P, Satish P, Jayasree Rajendran R, Rath HM, Sharma R. Safety and Efficacy of Novel Agents: Pelacarsen, Obicetrapib, and Beyond. Indian J Cardiovasc Dis Women. 2025;10:334-9. doi: 10.25259/IJCDW_66_2025

Abstract

Cardiovascular disease remains the leading global cause of mortality. Residual atherosclerotic risk persists despite intensive low-density lipoprotein cholesterol (LDL-C) lowering, in part due to genetically determined lipoprotein(a) [(Lp(a)}. Strong associations exist between increased atherogenic lipoproteins and cardiovascular risk. Although Lp(a) is an independent risk factor, most international guidelines have not yet endorsed therapeutic lowering of plasma Lp(a), while novel, non-statin agents now show promising reductions in Lp(a). Lifestyle and traditional therapies exert minimal effects on Lp(a); however, ribonucleic acid (RNA)-targeted agents and selective cholesteryl ester transfer protein (CETP) inhibition show substantial promise. Multiple RNA-based therapeutics are in development – most advanced is the antisense oligonucleotide pelacarsen (Phase 3, Lp(a)HORIZON). Obicetrapib, a highly selective CETP inhibitor, further lowers LDL-C and apoB when added to maximally tolerated therapy. This chapter reviews Lp(a) biology, epidemiology, clinical measurement, and the evidence base for emerging Lp(a)-lowering therapies (pelacarsen, olpasiran, lepodisiran, zerlasiran, and muvalaplin) as well as obicetrapib and advanced triglyceride-lowering agents. Practical pathways for screening and implementation in preventive cardiology are provided.

Keywords

Angiopoietin-like protein 3

Apolipoprotein C-3

Lepodisiran

Lipoprotein(a)

Muvalaplin

Obicetrapib

Olpasiran

Pelacarsen

Triglycerides

Zerlasiran

Show Related Articles from PubMed

INTRODUCTION

Cardiovascular disease (CVD) accounts for ~18 million deaths annually worldwide. Intensive low-density lipoprotein cholesterol (LDL-C) lowering remains central to event reduction, but residual risk is common – particularly among patients with elevated lipoprotein(a) [(Lp(a)], a causal, inherited risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis.^[1-4] Elevated Lp(a) is not meaningfully modified by diet or exercise, and currently approved pharmacotherapies offer only modest reductions, motivating outcomes-focused trials of novel agents.^[1-4]

LP(A): STRUCTURE, BIOLOGY, AND PATHOPHYSIOLOGY

Structure: Lp(a) is an apoB-100–containing LDL-like particle covalently linked through a disulfide bond to apolipoprotein(a) [apo(a)]. Oxidized phospholipids associate with both apoB and apo(a).^[1]

Mechanisms: Lp(a) promotes atherothrombosis through pro-inflammatory signaling, pro-atherogenic lipid deposition, and anti-fibrinolytic activity attributed to apo(a), accelerating plaque growth and calcification, including in the aortic valve.^[1-4]

Determinants and variability. Lp(a) levels are highly heritable and generally stable across life but may shift with thyroid, liver, or kidney disease; acute systemic inflammation; menopause; and hypogonadism. Levels can rise for up to 6 months post-myocardial infarction (MI).^[5-8]

EPIDEMIOLOGY AND RISK

Elevated Lp(a) (commonly >125 nmol/L or >50 mg/dL) confers independent risk of ASCVD events and aortic stenosis.^[2,3] Observational and genetic studies (including Mendelian randomization) suggest that large absolute reductions (≈>50–100 mg/dL) may be required for clinically meaningful event reduction over ~5 years. Population distributions differ by ancestry and sex; levels are often higher in Black individuals and in women.^[7-19]

CLINICAL MEASUREMENT AND SCREENING STRATEGY

Who to test ?

When to test and repeat. Because Lp(a) is largely genetically determined, one measurement is often sufficient; repeat testing may be considered post-MI (≥6 months) and post-menopause in women, or when secondary causes arise or are treated [Table 1].^[5-8]

Table 1: Whom and when to test for dyslipidemia

Premature ASCVD or strong family history of ASCVD
Personal history of ASCVD out of proportion to traditional risk factors
Suspected familial hypercholesterolemia
Recurrent events despite optimal LDL-C control
Repeat post-MI >6 months
Repeat post-menopause
Repeat when secondary causes arise, for example, thyroid disease

ASCVD: Atherosclerotic cardiovascular disease, LDL-C: Low-density lipoprotein cholesterol, MI: Myocardial infarction

CURRENT THERAPIES AND THEIR LIMITATIONS

Niacin and PCSK9 inhibitors modestly lower Lp(a), typically insufficient to reach the >50–100 mg/dL reduction hypothesized for event reduction. PCSK9-mediated Lp(a) lowering may diminish as baseline Lp(a) rises; inclisiran has shown ~20% reductions in elevated-Lp(a) subgroups [Table 2].^[2-4] Lipoprotein apheresis acutely reduces Lp(a) and may improve symptoms in select patients with recurrent cardiovascular events and very high Lp(a), but access, cost, and the need for repeated procedures limit widespread use.

Table 2: Summary of lpa lowering drug trials

Summary of LPA lowering drug trials
S. No.	Drug	Phase	Comments	Mechanism of action
1.	Pelacarsen	3	The Lp(a) HORIZON(a) trial is phase 3 trial , results expected in 2026, and if positive, it will give get the approval of first-in-class drug therapy specifically targeting elevated Lp(a) levels.	GalNAc-conjugated ASO binds to the mRNA transcript of the LPA gene, destroys it , and thus inhibits apo(a) - Apolipoprotein A synthesis in the liver
2.	Olpasiran	3	The results of the Lp(a) HORIZON(a) and OCEAN (a)-Outcomes are pending	First-in-class siRNA agent which is also GalNAc conjugated and prevents apo(a) synthesis.
3.	Lepodisiran	3	“-ACCLAIM-Lp(a)” will involve approximately 12,500 patients with ASCVD risk factors and with a baseline Lp(a) level ≥ 175 nmol/L. First study with Lp(a)-targeted therapy that has a primary prevention arm.	GalNAc-conjugated siRNA that was reported to produce durable reductions in Lp(a) levels
4.	Zerlasiran	2, 3 assumed to be in planning	Zerlasiran was well-tolerated and reduced Lp(a) concentration by 80% Trial Registration ClinicalTrials.gov Identifier: NCT05537571	19-mer siRNA, is also being covalently linked to the tri-antennary GalNac moiety.
5.	Muvalaplin	2, 3 being planned	Orally administered, lower price, and convenience, may improve patient adherence.	ASO-and siRNA-based therapies.

ASCVD: Atherosclerotic cardiovascular disease, Lp(a): Lipoprotein(a), ASO: Antisense oligonucleotide, siRNA: Small interfering RNA, GalNAc: N-acetylgalactosamine

6RNA-TARGETED LP(a)-LOWERING THERAPIES

Pelacarsen (antisense oligonucleotide [ASO]; N-acetylgalactosamine [GalNAc]-conjugated)

Mechanism: Pelacarsen binds LPA messenger RNA (mRNA) in hepatocytes, leading to RNase-mediated degradation and reduced apo(a) synthesis.^[15-18] Efficacy. Phase 2b and dose-ranging randomized controlled trials demonstrate ~25– 85% Lp(a) reductions (single dose) and ~59–82% (multiple ascending doses), sustained through day 113; ≥80% reductions have been consistently observed.^[16-18] Safety. Early-phase data reported no excess in injection-site reactions, serious adverse events, influenza-like illness, or discontinuations. Outcomes trial. Lp(a)HORIZON is an event-driven Phase 3 cardiovascular outcomes trial; topline results are expected in 2026.^[19] Epidemiologic context. Higher Lp(a) has been noted in Black populations and in women, with associations to peripheral artery disease and multi-vessel coronary artery disease (CAD). Given the burden of premature CAD in South Asians, this may be the first available therapy to reduce genetically mediated cardiovascular risk.^[7-9]

Olpasiran (small interfering RNA [siRNA]; GalNAc-conjugated)

Reduces apo(a) synthesis by degrading LPA mRNA. Phase 3 OCEAN(a)-OUTCOMES is ongoing.^[2,3]

Lepodisiran (siRNA; GalNAc-conjugated)

Phase 3 ACCLAIM-Lp(a) (~12,500 patients with ASCVD or high risk; baseline Lp(a) ~12,5nmol/L) includes a primary-prevention arm; durable Lp(a) reductions observed in earlier studies.^[4]

Zerlasiran (siRNA)

Completed phase 2 with >80% Lp(a) reduction over 36 weeks in ASCVD; phase 3 progression anticipated.^[5]

Muvalaplin (oral small molecule)

First-in-class oral Lp(a) inhibitor in Phase 2 with Phase 3 planning; an option that may improve access and adherence.^[6] Clinical note. Intra-individual Lp(a) variability is modest in the absence of acute illness; serial data from OCEAN(a)-DOSE help anchor expectations for monitoring.^[7]

CHOLESTERYL ESTER TRANSFER PROTEIN (CETP) INHIBITION REVISITED: OBICETRAPIB

Rationale: CETP inhibitors target the CETP enzyme, increasing high-density lipoprotein cholesterol (HDL-C) and decreasing LDL-C. Unlike prior CETP inhibitors with off-target effects, obicetrapib is highly selective, lowering LDL-C, apoB, non-HDL-C, and Lp(a) while raising HDL-C. BROADWAY (n = 2,530; ASCVD/HeFH). Obicetrapib 10 mg daily reduced LDL-C by 29.9% at day 84 versus +2.7% with placebo; also lowered Lp(a) and apoB; and increased HDL-C and apoA-I, with no signal for hepatic, muscle, or glycemic toxicity. TANDEM (n = 407). Fixed-dose obicetrapib 10 mg + ezetimibe 10 mg outperformed either monotherapy (LDL-C change at day 84: −48.6% combination vs. −27.9% ezetimibe vs. −16.8% obicetrapib) with similar adverse-event rates – supporting early fixed-dose combination in high-risk prevention. Meta-analytic signal. Pooled analyses suggest dose-dependent LDL-C lowering and HDL-C raising, potentiated by ezetimibe Table 3.^[7]

Table 3: Novel drugs for other types of dyslipidemias

S. No.	Drug	Phase	Comment	Mechanism of action
1.	Plozasiran	FDA approved	ApoC 3 inhibitor	SiRNA against ApoC3
2.	Volanesorsen	3	Reduction in TG levels were ~ 50% after 3 months of treatment and 10–38% after 21 months of treatment. Side effects of pancreatitis (74% reduction from previous) and platelet decline observed. Rejected by FDA but approved in UK	ASO Blocks apo-CIII synthesis in the nucleus by inhibiting APOC3 mRNA
3.	Olezarsen	2, five phase 3 trials are ongoing	Five phase 3 studies are currently ongoing with olezarsen in patients with either FCS or sHTG (> 500 mg/dL) or with TG between 150 and 500 mg/dL (moderate HTG) and ASCVD or at increased risk of ASCVD. FDA approved “Tryngolza”	advanced form of volanesorsen since this ASO is conjugated with N-acetylgalactosamine-improves delivery to the liver
4.	ARO-APOC3	2b, 3 trials ongoing	There are 3 currently ongoing trials with ARO-APOC3, with moderate HTG (NCT04998201), sHTG (>500 mg/dL) (NCT04720534), and FCS (NCT05089084)	GalNAc-conju gated siRNA that targets APOC3 mRNA.
5.	ARO-ANG3	One phase 2b and another phase 2 trial ongoing	There are currently 2 ongoing trials with ARO-ANG3, one with mixed dyslipidemia and other with HoFH	siRNA targeting ANGPTL3.
6.	Pegozafermin	2	Pegozafermin substantially reduced TGs after 8 weeks of therapy across all dose groups placebo-corrected changes from baseline ranging from −29.0% to −52.9%.	Long-acting glycopegylated analog human fibroblast growth factor 21, is in development for the treatment of sHTG and nonalcoholic steatohepatitis.
7.	Evinacumab	2	The primary end point was the mean percent reduction in triglycerides from baseline after 12 weeks of evinacumab exposure in cohort 3. Evinacumab reduced triglycerides in cohort 3 by a mean (S.E.M.) of −27.1% (37.4) (95% confidence interval −71.2 to 84.6), but the prespecified primary end point was not met. No notable differences in adverse events between evinacumab and placebo treatment groups were seen during the double-blind treatment period. • Evinacumab is also used in FH for LDL receptor independent lowering	Fully human monoclonal antibody that inhibits ANGPTL3. LOF variants in the gene encoding ANGPTL3 (ANGPTL3) have markedly reduced triglyceride

FDA: Food and Drug Administration, APOC3: Apolipoprotein C-3, SiRNA: Small interfering RNA, TG: Triglycerides, ASO: Antisense oligonucleotide, FCS: Familial chylomicronemia syndrome, HTG: Hypertriglyceridemia , ASCVD: Atherosclerotic cardiovascular disease, sHTG: Severe hypertriglyceridemia, ANGPTL3: Angiopoietin-like protein 3, HoFH: Homozygous familial hypercholesterolemia, FH: Familial hypercholesterolemia, LOF: Loss-of-function, LDL: Low-density lipoprotein, GalNAc: N-acetylgalactosamine, S.E.M: Standard error of the mean, mRNA: Messenger RNA

TRIGLYCERIDE-LOWERING AGENTS RELEVANT TO PREVENTION

Elevated triglycerides (TG) mark increased remnant particles and residual cardiovascular risk; severe hypertriglyceridemia (HTG) increases pancreatitis risk. Lifestyle is foundational; icosapent ethyl, statins, and fibrates offer additive benefit. In familial chylomicronemia syndrome (FCS) and multifactorial chylomicronemia syndrome, advanced agents targeting apolipoprotein C-3 (APOC3) and angiopoietin-like protein 3 (ANGPTL3) offer robust TG lowering:

Plozasiran (siRNA, APOC3): FDA-approved for FCS (PALISADE).^[9,12]
Volanesorsen (ASO, APOC3): ~50% TG reduction at 3 months; 10–38% at 21 months; pancreatitis reduction ~74% versus pre-treatment; thrombocytopenia signal; approved in UK.^[10]
Olezarsen (Tryngolza) (GalNAc-ASO, APOC3): FDA-approved; Phase 3 programs span FCS, severe HTG (>500 mg/dL), and moderate HTG (150–500 mg/dL) with ASCVD risk.^[11]
ARO-APOC3 (siRNA, APOC3): Phase 2b–3 in moderate/severe HTG and FCS.^[12]
ARO-ANG3 (siRNA, ANGPTL3): Phase 2 programs in mixed dyslipidemia and HoFH; severe HTG trial planned.^[13]
Pegozafermin (FGF21 analog): Placebo-corrected TG reductions ~29–53% at 8 weeks; in development for severe HTG and NASH.^[14,15]
Evinacumab (mAb, ANGPTL3): ~27% TG reduction in one cohort; primary TG endpoint not met; used for LDL-C lowering in familial hypercholesterolemia through LDL receptor-independent mechanisms.^[1]

SPECIAL POPULATIONS AND PRACTICAL CONSIDERATIONS

High-risk primary prevention: Individuals with LDL-C at target but high Lp(a) may benefit from outcomes-trial participation or investigational therapy when available. Women: Consider repeat Lp(a) after menopause if first measured earlier. Post-MI: Avoid interpreting acute elevations; defer retesting to ≥6 months post-event. Chronic kidney disease: Elevated Lp(a) compounds risk; integrate with statin/ezetimibe/PCSK9 therapy.^[6] Ancestry and equity: Higher Lp(a) distributions in Black populations underscore the need for equitable testing and trial access.^[7-9]

IMPLEMENTATION PATHWAY IN PREVENTIVE CLINICS

A one-time Lp(a) measurement is recommended in all adults [Figure 1].^[17] Risk flag: Premature ASCVD, strong family history, or events out of proportion to LDL-C burden. Measure Lp(a): Prefer nmol/L; document assay method. Optimize background lipid-lowering foundation: high-intensity statin ± ezetimibe; consider PCSK9 when indicated; address TGs (lifestyle, icosapent ethyl; consider advanced agents in severe HTG).^[8] Consider referral to clinical trials for markedly elevated Lp(a) with residual risk. Follow-up: If acute illness or MI, retest at appropriate intervals; reassess global risk and intensify non-Lp(a) risk-factor control.^[18]

Structural schematic of lipoprotein(a) [Lp(a)]

FUTURE DIRECTIONS

Event-driven outcomes from Lp(a)-specific RNA therapeutics (Lp(a)HORIZON; OCEAN(a)-OUTCOMES; and ACCLAIM-Lp(a)) will determine clinical adoption. Oral inhibition (muvalaplin) could broaden access. Key unanswered questions include optimal thresholds, duration, antithrombotic interactions, and effects in aortic stenosis.

CONCLUSION

Elevated Lp(a) is a causal, inherited driver of residual ASCVD risk not addressed by lifestyle or standard therapies.
Screen once in all adults (or at least in those at high ASCVD risk); repeat selectively after MI (≥6 months), after menopause, or when secondary conditions change.
RNA-targeted agents (pelacarsen, olpasiran, lepodisiran, and zerlasiran) lower Lp(a) by ~60–90% in trials; outcomes data are pending.
Obicetrapib adds potent LDL-C and apoB lowering with modest Lp(a) reduction and synergy with ezetimibe.
Advanced TG-lowering agents targeting APOC3/ANGPTL3 address another facet of residual risk.
Implementation today centers on identifying high Lp(a), optimizing LDL-C/TG management, and trial referral.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

Patient’s consent was not required as there are no patients in this study.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Financial support and sponsorship: Nil.

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