Plazomicin was found to be noninferior to meropenem. History
The drug was developed by the biotech company Achaogen. In 2012, the U.S. Food and Drug Administration granted fast track designation for the development and regulatory review of plazomicin. The FDA approved plazomicin for adults with complicated UTIs and limited or no alternative treatment options in 2018. Achaogen was unable to find a robust market for the drug, and declared bankruptcy a few months later. A generic version is manufactured by Cipla USA. Synthesis
It is derived from sisomicin by appending a hydroxy-aminobutyric acid substituent at position 1 and a hydroxyethyl substituent at position 6. The latter makes it impervious to acetylation (deactivation) by Aminoglycoside Acetyltransferase 6-N- Type Ib (AAC(6)-Ib), the most prevalent AAC enzyme. Names
Plazomicin is the international nonproprietary name (INN). References
Further reading
"FDA Briefing Information for the May 2, 2018 Meeting of the Antimicrobial Drugs Advisory Committee" (PDF). U.S. Food and Drug Administration. 2 May 2018. Retrieved 14 September 2019. "Achaogen Briefing Information for the May 2, 2018 Meeting of the Antimicrobial Drugs Advisory Committee" (PDF). U.S. Food and Drug Administration. 2 May 2018. Retrieved 14 September 2019. "Errata to the Achaogen Briefing Information for the May 2, 2018 Meeting of the Antimicrobial Drugs Advisory Committee" (PDF). U.S. Food and Drug Administration. 2 May 2018. Retrieved 14 September 2019. External links
"Plazomicin". Drug Information Portal. U.S. National Library of Medicine. "Plazomicin sulfate". Drug Information Portal. U.S. National Library of Medicine.
Recent research has shown that a mutation in the SOD1 gene is a risk factor for developing degenerative myelopathy in several breeds. Mutations in SOD1 are also associated with familial amyotrophic lateral sclerosis (Lou Gehrigs disease) in people. More than 100 SOD1 gene mutations are involved in human familial amyotrophic lateral sclerosis (ALS), and the pathologic spinal lesions of ALS are similar to those of canine DM, making canine DM a potentially useful animal model of ALS. Known causes of spinal cord dysfunction should be excluded before accepting the diagnosis of degenerative myelopathy;  disc disease (protrusions) or spinal cord tumors can cause compression of the spinal cord with similar signs to degenerative myelopathy. Treatment
Degenerative myelopathy is an irreversible, progressive disease that cannot currently be cured. There are no treatments that have been clearly shown to stop or slow progression of DM. Exercise
Exercise has been recommended to maintain the dogs ability to walk. Physiotherapy may prolong the length of time that the dog remains mobile and increase survival time. Canine hydrotherapy (swimming) may be more useful than walking. Use of a belly sling or hand-held harness allows the handler the ability to support the dogs hind legs for exercising or going up and down stairs. A 2-wheel dog cart, or "dog wheelchair" can allow the dog to remain active and maintain its quality of life once signs of weakness or paralysis of the hind limbs is detected. Prognosis
The prognosis for the disease is generally poor.