lincosamide

Clindamycin Phosphate is the phosphate salt form of clindamycin, a semi-synthetic, chlorinated broad-spectrum antibiotic produced by chemical modification of lincomycin. Clindamycin phosphate (Clindamycin 2-dihydrogen phosphate) is used in topical preparations.

Clindamycin (Sobelin) dissociates peptidyl-tRNA from the bacterial ribosome, thereby disrupting bacterial protein synthesis. Clindamycin is a semisynthetic broad-spectrum antibiotic produced by chemical modification of the parent compound lincomycin.

Lincomycin hydrochloride (U10149A) is a lincosamide antibiotic identified in S.lincolnensis with activity against gram-positive cocci and anaerobic bacteria.

Lincomycin (U-10149) is a lincosamide antibiotic from Streptomyces that is effective against most susceptible gram-positive and cell wall-less bacteria and is generally used in patients for whom penicillin is not available.

Quinupristin is a member of the macrolide-lincosamide-streptogramin class of antibiotics. Quinupristin blocks peptide bond synthesis to prevent the extension of polypeptide chains and promote the detachment of incomplete protein chains in the bacterial ribosomal subunits[1] [2].

Lincomycin-B is a lincosamide antibiotic isolated from the actinomycete Streptomyces lincolnensis.

Lincosamine is a lincosamide antibiotic produced by Streptomyces lincolnensis.

Clindamycin palmitate hydrochloride (Clindamycin palmitate HCl) is a water soluble hydrochloride salt of the ester of clindamycin and palmitic acid and a lincosamide antibiotic.

Clindamycin phosphate hydrochloride (Clindamycin 2-phosphate), a broad-spectrum bacteriostatic lincosamide antibiotic, serves as a prodrug of Clindamycin. It lacks antimicrobial activity in vitro; however, through phosphatase ester hydrolysis, it is rapidly converted to the active form, Clindamycin, in vivo. This compound is utilized in the research of acne and bacterial vaginosis [1] [2] [3].

Clindamycin-d3 (hydrochloride) is the deuterated form of Clindamycin. Clindamycin is an orally active, broad-spectrum lincosamide antibiotic that efficiently inhibits bacterial protein synthesis. It can suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Resistance to Clindamycin arises from the enzymatic methylation of the antibiotic binding site on the 50S ribosomal subunit (23S rRNA). It also reduces the production of leukocidin (PVL), toxic shock syndrome toxin-1 (TSST-1), and α-hemolysin (Hla). Additionally, Clindamycin is utilized in malaria research.