The pharmacological research of cisatracurium and the other individual isomers was then developed further primarily by R. Brandt Maehr and William B. Wastila, PhD (both of whom were pharmacologists within the Division of Pharmacology at Burroughs Wellcome Co.) in collaboration with John J. Savarese MD (who at the time was an anesthesiologist in the Dept. of Anesthesia, Harvard Medical School at the Massachusetts General Hospital, Boston, MA). Thereafter, the entire clinical development of cisatracurium was completed in a record short period from 1992 to 1994: the team of scientists was led by J. Neal Weakly PhD, Martha M. Abou-Donia PhD, and Steve Quessy PhD, in the Division of Clinical Neurosciences at Burroughs Wellcome Co., Research Triangle Park, NC. By the time of its approval for human use, in 1995, by the US Food and Drug Administration, Burroughs Wellcome Co. had merged with Glaxo Inc., and cisatracurium was approved to be marketed as Nimbex by GlaxoWellcome Inc. The trade name "Nimbex" was derived from inserting an "i" to the original proposal "Nmbex," which stood for excellent Neuromuscular blocker. Preclinical pharmacology
In vitro studies using human plasma indicated that cisatracurium spontaneously degrades at physiological pH via Hofmann elimination to yield laudanosine and the quaternary monoacrylate. Subsequent ester hydrolysis of the monoacrylate generates the monoquaternary alcohol, although the rate-limiting step is Hofmann elimination. In rat plasma, cisatracurium is also metabolized by non-specific carboxylesterases (a rate-limiting step) to the monoquaternary alcohol and the monoquaternary acid.
A delayed hemolytic transfusion reaction (DHTR) is a type of transfusion reaction. According to the Centers for Disease Controls (CDC) National Healthcare Safety Networks (NHSN) Hemovigilance Module, it is defined as:

Mechanism
If a person without a Kidd blood antigen (for example a Jka-Jkb+ patient) receives a Kidd antigen (Jka-antigen for example) in a red blood cell transfusion and forms an alloantibody (anti-Jka); upon subsequent transfusion with Jka-antigen positive red blood cells, the patient may have a delayed hemolytic transfusion reaction as their anti-Jka antibody hemolyzes the transfused Jka-antigen positive red blood cells. Other common blood groups with this reaction are Duffy, Rhesus and Kell. Diagnosis
Positive direct antiglobulin test (DAT) for antibodies developed between 24 hours and 28 days after cessation of transfusion
Positive elution test with alloantibodies present on the transfused red blood cells OR newly identified red blood cell alloantibodies in recipient serum.Antibody elution is the process of removing antibodies from the surface of red blood cells. Techniques include using heat, ultrasound, acids or organic solvents. No single method is best in all situations. In an elution test, the eluted antibodies are subsequently tested against a panel of reagent red blood cells of known phenotype. Inadequate rise of post-transfusion hemoglobin level OR rapid fall in hemoglobin level back to pre-transfusion levels OR otherwise unexplained appearance of spherocytes.PROBABLE DIAGNOSIS

Newly identified red blood cell alloantibody demonstrated between 24 hours and 28 days after cessation of transfusion BUT incomplete laboratory evidence to meet definitive case definition criteria.