EVKEEZA® is the first and only approved ANGPTL3 inhibitor that lowers LDL-C independently of LDLR activity1
- Patient with HoFH
- with evkeeza
Patients with HoFH have increased LDL-C due to diminished or absent LDLR function
- ANGPTL3, an angiopoietin-like protein, plays a prominent role in the regulation of lipid metabolism by inhibiting lipoprotein lipase (LPL) and endothelial lipase (EL).1,2
- Some clearance is still possible through VLDL remnant receptors.1,2
- Diminished/absent LDLR function prevents the LDL clearance, thereby increasing LDL-C levels.1,2
Evinacumab inhibition of ANGPTL3 leads to reduction in LDL-C, HDL-C, TG and ApoB.
EVKEEZA binds to and inhibits ANGPTL3, reducing LDL-C levels in an LDLR-independent manner1,2
- EVKEEZA binds to and inhibits ANGPTL3.1,2
- By inhibiting ANGPTL3 with EVKEEZA, the activity of LPL and EL is restored, resulting in clearance of VLDL remnants via remnant receptors in the liver.1,2
- By enhancing VLDL remnant clearance, EVKEEZA reduces LDL-C levels in an LDLR-independent manner.1,2
Evinacumab inhibition of ANGPTL3 leads to reduction in LDL-C, HDL-C and TG.
See how EVKEEZA inhibits ANGPTL3 to lower LDL-C
ANGPTL3=angiopoietin-like 3; LDL-C=low-density lipoprotein cholesterol; LDLR=LDL-receptor; HoFH=homozygous familial hypercholesterolemia; EL=endothelial lipase; LPL=lipoprotein lipase; VLDL=very low-density lipoprotein; HDL-C=high-density lipoprotein cholesterol; TG=triglycerides; IDL=intermediate-density lipoprotein.
References:
- EVKEEZA Product Monograph. Ultragenyx Pharmaceutical, Inc. 2023.
- Adam RC, Mintah IJ, Alexa-Braun CA, et al. Angiopoietin-like protein 3 governs LDL-cholesterol levels through endothelial lipase-dependent VLDL clearance. J Lipid Res. 2020;61(9):1271-1286.
