Table 2: Summary of Emerging Triglyceride-lowering Therapies.

Therapeutic agent	Mechanism of action	Lipid modification effects	Impact on cardiovascular system
Pemafibrate[97]	Selective PPARα modulator	↓TG ↓VLDL ↓RLP-C and ↓ApoC-III	Decrease atherogenic lipoprotein levels[99]
AKCEA-ANGPTL3-LRx[103] (vupanorsen, evinacumab)	Vupanorsen is ASOs therapy targeting Angptl3 (mRNA) Evinacumab is a monoclonal antibody that targets another therapeutic modality, which has been developed to inhibit ANGPTL3	↓ApoC-III ↓TRL ↓TG ↓ApoB, ↓Non-HDL-C, ↓VLDL-C ↑HDL-C	Attenuate the progression of atherosclerosis[102]
AKCEA-ApoCIII-LRx[109,116] (volanesorsen, olezarsen)	Antisense oligonucleotide that reduces the production of ApoC-III	↓TRL ↓TG ↓LDL-C ↑HDL-C	Decrease atherogenic lipoproteins in patients with moderate hypertriglyceridemia and at high risk for or with established cardiovascular disease[109,116]
Lomitapide[110]	MTP inhibitor that reduces the synthesis of VLDL	↓TRL ↓TG ↓LDL-C ↑HDL-C	Decrease plasma levels of atherogenic lipoproteins in patients with HoFH[112]

ANGPTL3 = angiopoietin-like protein 3; ApoB = apolipoprotein B; ApoC-III = apolipoprotein C-III; ASOs = antisense oligonucleotide; HoFH = homozygous familial hypercholesterolemia; IDL = intermediate-density lipoprotein; LDL-C = LDL cholesterol; MTP = microsomal triglyceride transfer protein; Non-HDL-C = non-HDL cholesterol; PPARα = peroxisomal proliferator activated receptor-alpha; RLP-C = remnant lipoprotein cholesterol; TRL-C = triglyceride-rich lipoprotein; TG = triglyceride; VLDL = very LDL; VLDL-C = very LDL cholesterol.