A neutralizing APOA5 monoclonal antibody reduces amounts of lipoprotein lipase in capillaries and triggers hypertriglyceridemia

Y Ye Yang A Anne P. Beigneux (Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles) T Troy L. Lowe (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) Y Yan Q. Chen (Lilly Research Laboratories, Eli Lilly and Company) K Katherine Xie (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) H Hyesoo Jung (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) Y Yiping Tu (Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles) R Rachel G. Yu (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) J Julia L. Scheithauer (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) S Shailen Mehta (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) J Jerry Wu (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) L Lindsay Alvarez (Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles) W W. Sean Davidson G Gabriel Birrane (Division of Experimental Medicine, Beth Israel Deaconess Medical Center) A Alan T. Remaley (Laboratory of Lipoprotein Metabolism, Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH) D Denis Sviridov (Laboratory of Lipoprotein Metabolism, Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH) M Michael Ploug (Finsen Laboratory, Copenhagen University Hospital - Rigshospitalet) E Eugene Y. Zhen (Lilly Research Laboratories, Eli Lilly and Company) Y Yuewei Qian (Lilly Research Laboratories, Eli Lilly and Company) J John H. Sloan (Lilly Research Laboratories, Eli Lilly and Company) R Robert W. Siegel (Laboratory for Experimental Medicine, Lilly Research Laboratories, Eli Lilly and Company) R Robert J. Konrad (Lilly Research Laboratories, Eli Lilly and Company) L Loren G. Fong (Department of Medicine, David Geffen School of Medicine, University of California Los Angeles) S Stephen G. Young (Department of Medicine, David Geffen School of Medicine, University of California Los Angeles)

Abstract

Apolipoprotein AV (APOA5) regulates intravascular triglyceride metabolism by binding to the angiopoietin-like protein 3/8 complex (ANGPTL3/8) and suppressing its ability to unfold the native conformation of lipoprotein lipase (LPL). LPL unfolding results in loss of catalytic activity and the detachment of LPL from the surface of cells. An APOA5 truncation mutation (identified in two patients with hypertriglyceridemia) had suggested that the last 35 amino acids of APOA5 are important for its function. We reasoned that a monoclonal antibody (mAb) against carboxyl-terminal sequences in APOA5 could clarify functionally important amino acid residues in APOA5 and assist in elucidating the mechanism by which APOA5 regulates plasma triglyceride metabolism. Because carboxyl-terminal APOA5 sequences are evolutionarily conserved, we began by screening a human Fab bacteriophage library for binders of carboxyl-terminal APOA5 sequences. We identified one such binder and used phage DNA sequences to build a chimeric IgG 1 mAb (IBA707) against APOA5. The binding of IBA707 to APOA5 was abolished by nonconservative amino acid substitutions in conserved sequences (residues L337–I348) within a C-terminal α-helix in APOA5. The same substitutions disrupted APOA5’s ability to bind and inhibit ANGPTL3/8 activity. IBA707-mediated blockade of APOA5 function reduced intracapillary LPL levels and triggered elevated plasma levels of triglycerides and ANGPTL3/8 in both fasted and refed mice. IBA707 was cleared rapidly from the plasma in Apoa5 +/+ mice but slowly in Apoa5 –/– mice. Our studies identified functionally important amino acids in APOA5 and revealed that APOA5 controls plasma triglyceride metabolism in part by modulating plasma levels of ANGPTL3/8.

Article Details

Volume / Issue Vol. 123, Issue 1
Published January 06, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (24)

Y

Ye Yang

A

Anne P. Beigneux

Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles

T

Troy L. Lowe

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

Y

Yan Q. Chen

Lilly Research Laboratories, Eli Lilly and Company

K

Katherine Xie

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

H

Hyesoo Jung

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

Y

Yiping Tu

Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles

R

Rachel G. Yu

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

J

Julia L. Scheithauer

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

S

Shailen Mehta

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

J

Jerry Wu

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

L

Lindsay Alvarez

Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles

W

W. Sean Davidson

G

Gabriel Birrane

Division of Experimental Medicine, Beth Israel Deaconess Medical Center

A

Alan T. Remaley

Laboratory of Lipoprotein Metabolism, Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH

D

Denis Sviridov

Laboratory of Lipoprotein Metabolism, Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH

M

Michael Ploug

Finsen Laboratory, Copenhagen University Hospital - Rigshospitalet

E

Eugene Y. Zhen

Lilly Research Laboratories, Eli Lilly and Company

Y

Yuewei Qian

Lilly Research Laboratories, Eli Lilly and Company

J

John H. Sloan

Lilly Research Laboratories, Eli Lilly and Company

R

Robert W. Siegel

Laboratory for Experimental Medicine, Lilly Research Laboratories, Eli Lilly and Company

R

Robert J. Konrad

Lilly Research Laboratories, Eli Lilly and Company

L

Loren G. Fong

Department of Medicine, David Geffen School of Medicine, University of California Los Angeles

S

Stephen G. Young

Department of Medicine, David Geffen School of Medicine, University of California Los Angeles