Review

Volume 17, Number 4, April 2025, pages 181-186

Lipoprotein(a)-Lowering Drugs: A Mini Review

Lipoprotein(a) (Lp(a)) is a unique type of lipoprotein consisting of low-density lipoprotein (LDL) and an apoprotein(a) (apo(a)) [1-5]. LDL, which carries apolipoprotein B (apoB), is known to be involved in atherogenesis, and apo(a) is a plasminogen-like protein that competes with plasminogen to inhibit its anti-thrombotic activity [1-3]. Apo(a) also stimulates a platelet-activating factor, which initiates angiogenesis, and binds to oxidized phospholipid (ox-PL)-rich LDL, which participates in the development of atherosclerosis [1, 3, 6, 7]. With such characteristics, Lp(a) exhibits pathophysiological relevance in cardiovascular disease (CVD) [8, 9].

Although the metabolism of Lp(a) is not completely understood, the majority of its synthesis and catabolism occurs in the liver, with only a minor part of the synthesis occurring in the intestine [10]. Apo(a) and apoB are produced in the nucleus, and LDL assembly occurs in the endoplasmic reticulum. Apo(a) binds to apoB of LDL on the cell surface [11], and Lp(a) is secreted from the liver into the bloodstream. Multiple pathways have been proposed for the catabolism of Lp(a), such as the binding of apo(a) to the LDL receptor or very-low-density lipoprotein receptor on hepatocytes and the binding of Lp(a) with ox-PL to CD36 or type B scavenger receptor on macrophages [12].

Blood Lp(a) levels show a skewed distribution towards higher concentrations, and Lp(a) < 30 mg/dL is often considered normal [4]. The Lp(a) level is primarily determined by genetic variations in apo(a) [3]. Genetic variation within the LPA gene results in the presence of kringle-like repeats, and a negative correlation has been observed between the length of this region and Lp(a) levels [3]. Single nucleotide polymorphisms (SNP) in the LPA gene affect kringle-like repeats, further affecting Lp(a) levels [13]. Lp(a) has also been positively associated with inflammation [4] because its expression of LPA gene is regulated by interleukin-6, an inflammatory molecule [14].

Even though cardiometabolic pathologies such as diabetes mellitus [15], renal kidney disease [16], and familial hypercholesterolemia [17] can modify blood Lp(a) levels, Lp(a) has been confirmed as an independent risk factor for CVD [8, 9]. In fact, guidelines recommend measuring Lp(a) levels to assess the risk of CVD [18, 19]. Lowering Lp(a) levels may reduce CVD risk [8, 9, 18, 19]. To meet this expectation, treatments that specifically control Lp(a) have recently emerged [20]. Such drugs greatly reduce Lp(a) levels using antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), or small molecule Lp(a)-formation inhibitors. To put this into perspective, we briefly summarize the treatments, including earlier attempts at reducing Lp(a).

Lipid-lowering drugs used in clinical practice include statins, fibrates, niacin, and other medications that mainly lower LDL-cholesterol (LDL-C) levels (Table 1) [14, 20-30]. Although these lipid-lowering therapies do not always focus on reducing Lp(a) levels, their effects on Lp(a) have been of interest. The functions of the drugs are partly known (Fig. 1).

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Table 1. Effects of Lipid-Lowering Drugs and Lp(a)-Specific Drugs on Lp(a)

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Figure 1. Lp(a) regulation by drugs; a simple schematic illustration. Bold arrow indicates acceleration; bold T-bar indicates inhibition. Since statins modulate both apoB synthesis and LDLR activation, resulting in a varied effect on Lp(a), they are not described in the figure. Apo(a): apolipoprotein(a); apoB: apolipoprotein B; ASO: antisense oligonucleotide; LDL: low-density lipoprotein; LDLR: low-density lipoprotein receptor; MTTP: microsomal triglyceride transfer protein; PCSK9: proprotein convertase subtilisin/kexin type 9; Lp(a): lipoprotein(a).

The effects of lipid-lowering drugs on Lp(a) levels depend on the mechanism of cholesterol reduction. Statins, which control cholesterol synthesis in the liver and LDL receptor uptake of LDL-C from the blood, are popular lipid-lowering drugs [21, 31]. The effect of statins on Lp(a) levels is reported to vary; basically, Lp(a) levels are not largely changed by statins. Fibrates are generally used to reduce triglycerides, while some associations are suggested between triglycerides and Lp(a) levels; actually, Lp(a) levels are unchanged or slightly increased by fibrates [22, 32]. Niemann-Pick C1-Like1 inhibitors control cholesterol absorption, which can reduce Lp(a) levels by approximately 7% [24, 34, 35].

Recently used LDL-specific drugs that inhibit LDL formation or uptake are typically used in a condition such as severe hypercholesterolemia. As proprotein convertase subtilisin/kexin type 9 (PCSK9) degrades LDL receptors and then increases LDL in circulation, PCSK9 inhibitors protect LDL receptors and accelerate the uptake of LDL with Lp(a) [36], resulting in a > 20% reduction in Lp(a) levels [25, 26, 37].

Microsomal triglyceride transfer protein (MTTP) inhibitors and apoB ASO prevent LDL-formation, and the respective drugs show 13% and 32% reduction in Lp(a) levels [27, 38-40].

In the period when Lp(a) levels are not specifically reduced, estrogen-related drugs and certain supplements have been considered to modulate these levels (Table 2) [41-46]. Understanding the mechanisms behind Lp(a) levels can enhance our knowledge of how to modulate its levels effectively.

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Table 2. Effects of Estrogen-Related Drugs and Supplements on Lp(a)

Estrogen-related drugs have been reported to significantly reduce Lp(a) levels (Fig. 1). Hormone replacement therapy (HRT) reduces Lp(a) levels by 20% [41]. The transcription factor, estrogen receptor α, is upregulated by binding to estrogen response element sites near the LPA gene, leading to the suppression of apo(a) synthesis [41]. Tibolone is known for menopausal hormone therapy and also reduces Lp(a) levels by 25% [42]. Among the anti-estrogen drugs, tamoxifen and raloxifene reduced Lp(a) levels by 0.40 mg/dL in male patients with hypercholesterolemia [43, 44].

Observing Lp(a) reduction in some supplements (Table 2) [41-46], L-carnitine has been reported to reduce Lp(a) levels by 8.82 mg/dL in patients with diabetes mellitus and hypercholesterolemia [45]. L-carnitine may potentially reduce Lp(a) by attenuating the stimulation of fatty acid breakdown, which is necessary for bile acid production [45]. Coenzyme Q10 has also been shown to reduce Lp(a) levels by 3.54 mg/dL in patients with both diabetes mellitus and hypercholesterolemia [46]. The attenuation of inflammation by coenzyme Q10 can lead to the reduction in Lp(a) [46].

The studies by Lp(a)-specific drugs are described in Table 1 [20, 28-30]. ASOs targeting apo(a) are designed to reduce apo(a) synthesis by inhibiting the silencing of apo(a) mRNA, which specifically reduces Lp(a), but not LDL (Fig. 1) [47, 48]. In a clinical trial [20], pelacarsen, an ASO conjugated with triantennary N-acetylgalactosamine specific to hepatocytes, using ligand-conjugated antisense technology, reduced Lp(a) levels by up to 47% in patients with high Lp(a) levels of ≥ 29 mg/dL (median: 82 mg/dL). Moreover, CVD risk reduction is assumed to be mediated by proinflammatory activation, as observed by a reduction in circulating monocytes [49]. Recently, a phase II study was conducted, and pelacarsen (20 mg per week) reduced Lp(a) levels by up to 80% over a 27-week period in CVD patients with high Lp(a) levels of ≥ 50 mg/dL (median: 87 mg/dL) [20]. The CVD outcomes, including the events and deaths, were not significantly affected by drug intervention because the intervention period was only 6 months, which appeared to be too short to observe the outcomes [20]. The clinical trial turned into a phase III study focusing on CVD outcomes over a period of several years. Similar apo(a)-targeting drugs using siRNAs are also being clinically tested. Olpasiran reduced Lp(a) levels by 40% in a phase II trial with high Lp(a) levels of ≥ 60 mg/dL (median: 104 mg/dL) [28]. The pre-clinical assessment of zerlasiran has been completed [50], showing a reduced Lp(a) levels by 90% in a phase II trial with high Lp(a) levels of ≥ 50 mg/dL (median: 85 mg/dL) [29].

Muvalaplin, a chemical compound, makes apo(a) non-functional [30] (Fig. 1). It binds the interaction site of apo(a) to apoB and inhibits the formation of Lp(a) [30, 51]. Muvalaplin was shown to reduce Lp(a) levels by 63-65% relative to placebo with high Lp(a) levels of ≥ 30 mg/dL (median: 58 mg/dL) [30]. The LDL-C level was not altered by muvalaplin treatment. Although this was only a phase I trial and did not reveal significantly lower Lp(a) levels, it is still of concern because it is the only oral Lp(a)-specific drug.

The overall summary of the treatments for Lp(a) reduction is listed in Table 1 (lipid-lowering drugs and Lp(a)-specific drugs) [14, 20-30] and Table 2 (estrogen-related drugs and supplements) [41-46]. In summary, recently developed Lp(a)-specific drugs, such as an apo(a) ASO, siRNAs, and Lp(a)-formation inhibitor, can have a greater effect on Lp(a) reduction. The fact that their effects are independent of LDL-C levels has received attention. Each 5-mg/dL reduction in Lp(a) levels is associated with a 2.5% relative CVD risk reduction [17, 52]. A great effect of Lp(a)-specific drugs to reduce CVD has been estimated, although up to now, a preceding trial using those drugs with a small population has not demonstrated their effect on CVD outcomes [20, 28, 29].

The threshold levels of Lp(a) for the development of CVD are also debatable [4]. Although Lp(a)-specific drugs have been used for patients with high Lp(a) levels [20, 28-30], the threshold (target) levels of Lp(a) for the prevention of CVD should be defined in the future. This would lead to a discussion regarding which patients are most likely to benefit from treatment and/or to whom treatments should be appropriately applied.

Here, an earlier attempt at lowering Lp(a) levels using lipid-lowering drugs, as well as estrogen-related drugs and supplements, has been reviewed. Recently developed Lp(a)-specific drugs, such as apo(a) ASO, siRNAs, and an Lp(a)-formation inhibitor, can have a greater effect on Lp(a) reduction. The effect of Lp(a) reduction on CVD outcomes is expected but remains unknown. Clinical trials using Lp(a)-specific drugs are ongoing, and additional data from such trials are needed to establish the benefits of treatment on CVD outcomes.

Acknowledgments

None to declare.

Financial Disclosure

No funding was received for this paper.

Conflict of Interest

MH also works at Eiken Chemical Co., Ltd. The other author declares no conflict of interest.

Author Contributions

Conceptualization: MH and KK. Writing - original draft preparation: MH. Writing - review and editing: KK. Supervision: KK. All authors have read and agreed to the published version of the manuscript.

Data Availability

The authors declare that data supporting the findings of this study are available within the article.

Abbreviations

Lp(a): lipoprotein (a); apo(a): apolipoprotein (a); apoB: apolipoprotein B; LDL: low-density lipoprotein; PCSK9: proprotein convertase subtilisin/kexin type 9; ASO: antisense oligonucleotide; siRNAs: small interfering RNAs

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