Clindamycin

Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria^[1][2]. IC50 & Target:MIC Tatget:Clindamycin^[4] MIC: 200 μg/mL (E. coli)^[4] In Vitro:Clindamycin (25 μg/mL, 1-18 h) inhibits ceftazidime (HY-B0593)-induced endotoxin release pretreatment in E. coli O55:B5^[3].
Clindamycin (50-100 μg/mL, 0-12 min) enhances antibody- and complement-dependent phagocytosis in Staphylococcus aureus^[4].
Clindamycin (0-500 μg/mL, 24-72 h) inhibits the cell proliferation in osteoblast cell culture model, stimulates the cell metabolism of osteoblast at the contratibution of 10 μg/mL^[5].
In Vivo:Clindamycin (50-300 mg/kg; i.v., p.o.) dosage doesn’t affect pharmacokinetic parameters in rats^[6].
Clindamycin (160-600 mg/kg; i.v.) improves survival in a dose-dependent manner in endotoxic shock mouse model^[7].
Clindamycin (17-50 mg/kg, i.v.) has good penetration into rat muscle tissue that can be applied to inhibit the main bacteria causing odontogenic infections^[8].

Pharmacokinetic Analysis in Rat Model^[8]

Route	Dose (mg/kg)	t1/2 (h)	Cmax (mg/mL)	Tmax (h)a	AUC0-inf (h.mg/L)	?T
i.v.	51(Plasma)	2.51 (2.37-2.83)	35.21 (25.04-42.65)	0.08 ± 0.00	44.78 (28.82-65.65)	/
i.v.	51(Tissue)	2.82 (2.57-3.05)	14.20 (10.63-14.89)	0.25 ± 0.00	16.54 (13.83-18.35)	1.10
i.v.	17(Tissue)	3.25 (3.13-3.44)	4.82 (3.35-6.66	0.25 ± 0.00	/	/