Ultimately, under their claims of breach of duty to warn and strict liability due to the plaintiffs citing risk of physical injury to others, not physical injury to themselves, the case was dismissed by the courts. Although the case was not certified as class action and their claims of breach of duty to warn and strict liability was dismissed, the courts did not dismiss the battery allegations. The issue was then to determine whether the University of Chicago had committed battery against these women but the case was settled before trial. Part of the settlement agreement for this case, Mink v. University of Chicago, attorneys for the plaintiffs negotiated for the university to provide free medical exams for all offspring exposed to DES in utero during the 1950 experiments as well as  treat the daughters of any women involved who develop DES-associated vaginal or cervical cancer.As of February 1991, there were over a thousand pending legal actions against DES manufacturers. There are over 300 companies that manufactured DES according to the same formula and the largest barrier to recovery is determining which manufacturer supplied the drug in each particular case. Many of the successful cases have relied on joint or several parties holding liability. A lawsuit was filed in Boston Federal Court by 53 DES daughters who say their breast cancers were the result of DES being prescribed to their mothers while pregnant with them. Their cases survived a Daubert hearing.
However, they also noted that the importance of the activities requires further study in animal models at pharmacologically relevant doses.DES has been identified as an antagonist of all three isotypes of the estrogen-related receptors (ERRs), the ERRα, ERRβ, and ERRγ. Half-maximal inhibition occurs at a concentration of about 1 μM. Pharmacokinetics
DES is well-absorbed with oral administration. With an oral dosage of 1 mg/day DES, plasma levels of DES at 20 hours following the last dose ranged between 0.9 and 1.9 ng/mL (3.4 to 7.1 nmol/L). Sublingual administration of DES appears to have about the same estrogenic potency of oral DES in women. Intrauterine DES has been studied for the treatment of uterine hypoplasia. Oral DES is thought to have about 17 to 50% of the clinical estrogenic potency of DES by injection.The distribution half-life of DES is 80 minutes. It has no affinity for SHBG or corticosteroid-binding globulin, and hence is not bound to these proteins in the circulation. The plasma protein binding of DES is greater than 95%.Hydroxylation of the aromatic rings of DES and subsequent conjugation of the ethyl side chains accounts for 80 to 90% of DES metabolism, while oxidation accounts for the remaining 10 to 20% and is dominated by conjugation reactions. Conjugation of DES consists of glucuronidation, while oxidation includes dehydrogenation into (Z,Z)-dienestrol. The medication is also known to produce paroxypropione as a metabolite. DES produces transient quinone-like reactive intermediates that cause cellular and genetic damage, which may help to explain the known carcinogenic effects of DES in humans.