TABLE 1.

Beta 2‐glycoprotein 1 as a molecular‐therapeutic target in APS‐related pregnancy morbidity

Therapy	ß2GP1 relation	Mechanism of action	Effect	Model	References
TIFI peptide	Mimics Vth domain of ß2GP1.	Competitive inhibition: prevents binding of ß2GP1 to target cells.	Dose ‐ dependent inhibition of ß2GP1 binding to trophoblast.	In vitro. Cytotrophoblast cell culture.	[95, 96, 97]
			Reduce growth retardation and fetal loss rate induced by aPL.	In vivo. Murine model, pregnant C57BL/6 mice.
1N11 monoclonal antibody	Monoclonal antibody to ß2GP1.	Decreases antibody binding to ß2GP1 and impede interaction between ß2GP1 and apoER2.	Prevents alterations of early trophoblast migration and proliferation.	In vitro. Trophoblast cell line HTR‐8SV neo.	[98]
			Reduce increase in fetal resorption induced by aPL.	In vivo. Murine model, female Balb/c.
MBB2ΔCH2	Non‐complement fixing antibody to ß2GP1.	Competitive inhibition: prevents binding of aß2GP1 to ß2GP1 domain I.	Reduce fetal resorption frequency and increase fetal weight.	In vitro. BeWo and HUVECs In vivo. Murine model‐ female BALB/c mice.	[99]

Abbreviations: aPL, antiphospholipid antibodies; apoER2, apolipoprotein E receptor 2; aß2GP1, antibodies anti beta 2‐glycoprotein‐1; HTR‐8SV. First‐trimester human trophoblast cells; HUVEC, human umbilical cord vein endothelial cells.;ß2GP1, beta 2‐ glycoprotein‐1.