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"Prevention of implantation" describes a physiological process whereby pregnancy is blocked by disruption of the embryo's ability to attach and invade the endometrial lining. Methods to prevent implantation include intrauterine devices (IUDs), which can be copper-based (inducing a local immune response) or hormonal (levonorgestrel, altering mucus and/or endometrial receptivity), and some emergency contraception drugs, though evidence that these act directly at implantation is weak. Progestin-only pills, combined oral contraceptives, and some injectable contraceptives mainly prevent ovulation or fertilization and rarely act by inhibiting implantation. "Prevention of implantation" is an effect or outcome, not a distinct molecular entity, so there is no canonical name, abbreviation, or molecular classification. Any "targeting" occurs via modification of endometrial environment, hormone-dependent changes, or immune modulation. No direct molecular biomarkers for "prevention of implantation" exist; endometrial thickness or markers of receptivity (e.g., LIF, integrins, matrix molecules) are sometimes monitored in fertility, not contraception.
These act by making the endometrium unreceptive to embryo implantation, altering uterine lining, or providing local immune responses toxic to sperm/ova or impeding blastocyst attachment.
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