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Clindamycin

MCE China：Clindamycin

Brand：MedChemExpress (MCE)

Cat. No.HY-B1455

CAS：18323-44-9

Purity：99.90%

Storage：-20°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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]. 1.19 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 / /

IC50 & Target：Plasmodium

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References：

[1]. Hodille E, et al. Clindamycin suppresses virulence expression in inducible clindamycin-resistant Staphylococcus aureus strains. Ann Clin Microbiol Antimicrob. 2018 Oct 20;17(1):38.  [Content Brief]

[2]. Kremsner PG. Clindamycin in malaria treatment. J Antimicrob Chemother. 1990 Jan;25(1):9-14.  [Content Brief]

[3]. Kishi K, et al. Clindamycin suppresses endotoxin released by ceftazidime-treated Escherichia coli O55:B5 and subsequent production of tumor necrosis factor alpha and interleukin-1 beta. Antimicrob Agents Chemother. 1999 Mar;43(3):616-22.  [Content Brief]

[4]. Veringa EM, et al. Clindamycin at subinhibitory concentrations enhances antibody- and complement-dependent phagocytosis by human polymorphonuclear leukocytes of Staphylococcus aureus. Chemotherapy. 1987;33(4):243-9.  [Content Brief]

[5]. Naal FD, et al. The effects of clindamycin on human osteoblasts in vitro. Arch Orthop Trauma Surg. 2008 Mar;128(3):317-23.  [Content Brief]

[6]. Yang SH, Lee MG. Dose-independent pharmacokinetics of clindamycin after intravenous and oral administration to rats: contribution of gastric first-pass effect to low bioavailability. Int J Pharm. 2007 Mar 6;332(1-2):17-23.  [Content Brief]

[7]. Hirata N, et al. Pretreatment of mice with clindamycin improves survival of endotoxic shock by modulating the release of inflammatory cytokines. Antimicrob Agents Chemother. 2001 Sep;45(9):2638-42.  [Content Brief]

[8]. Faggion PI, et al. Is the penetration of clindamycin into the masseter muscle really enough to treat odontogenic infections? Clin Oral Investig. 2021 May;25(5):3257-3266.  [Content Brief]