Teratogenicity
Teratogenicity is the capacity of an exposure to cause structural or functional abnormality in a developing embryo or fetus, and it depends sharply on timing, dose and susceptibility.
Teratogenicity describes an exposure that disturbs development rather than one that is simply toxic. Three variables govern it. Timing matters most, because organogenesis in humans runs roughly from the third to the eighth week after conception, when a brief exposure can produce a structural defect that the same exposure later would not. Dose matters, with thresholds below which no effect appears. And genotype matters, which is why species differ so markedly in what harms them.
Thalidomide is the case that built the modern system. Marketed from the late 1950s as a sedative and antiemetic, it caused characteristic limb reduction defects and was withdrawn in 1961, prompting the 1962 amendments to American drug law and the reproductive toxicology requirements now standard worldwide. Registration programmes today include embryo-fetal development studies conventionally run in two species, typically a rodent and the rabbit, with results reported as exposure multiples of the clinical dose.
Interpreting those studies is where judgement enters. A malformation seen only at exposures many times the therapeutic range means something different from one at clinically relevant exposure. Human data are usually absent at approval because pregnant participants are excluded from trials, so pregnancy exposure registries accumulate the real evidence slowly after launch.
A tempting and wrong argument is that large or charged peptides cannot be teratogens because they cross the placenta poorly. Placental transfer is not the only route to fetal harm: maternal weight loss, nutrient restriction, hyperthermia and altered maternal hormones all act indirectly, and antibody-based constructs are actively transported into the fetal circulation from the second trimester onward.