| DRUGS | MECHANISM OF ACTION | TOXICITY IN PREGNANCY | COMMENTS | CATEGORY US FDA |
| METHOTREXATE | Inhibits DNA synthesis by inhibition of folic acid reductase | Congenital malformations | Induces fetal death | X |
| HIDROXICLOROQUINE | The mechanisms that explain its immunomodulatory effect are unclear. | Teratogenic effects have not been proven. | Most used drug in which no effects have been shown in pregnancy | C |
| MYCOPHENOLATE | Blocks DNA synthesis through inhibition of IMPDH | Congenital malformation and losses 1st trimester | Its active metabolite is mycophenolic acid | D |
| TACROLYMUS | Calcineurin inhibitor inhibits T lymphocyte activation | Nephrotoxic at high doses, hypertension, gestational diabetes | Requires high doses to achieve effect and low serum levels to reduce nephrotoxicity | C |
| AZATHIOPRINE | Inhibits DNA synthesis by antagonism with purines | Intrauterine growth retardation | The fetus cannot metabolize the enzyme to its active 6-MMP form. | D |
| CYCLOPHOSPHAMIDE | Blocking DNA replication and RNA transcription through the formation of covalent bonds with alkyl groups | Fetal loss | Fetal death | D |
| ADALIMUMAB INFLIXIMAB | Chimeric monoclonal antibody inhibits tumor necrosis factor activity. | Not known toxicity | IgG molecules do not cross the placenta in the first trimester. Greater risk of infection. | B |
| RITUXIMAB | Monoclonal antibody antti CD20 reduces B lymphocytes | Neonatal cytopenia | IgG molecules do not cross the placenta in the first trimester | C |