Pharmacokinetics of COS

BZ Oligo

Pharmacokinetics (PK) describes the fate of a given compound in the body, including the absorption, distribution, metabolism and elimination. PK data provide insight into the kinetics of systemic exposure to a particular substance. In addition, PK profiles are useful for estimating therapeutically effective doses and for reflecting the pharmacological favorability of a particular substance. Accordingly, a number of studies have been performed to investigate the PK characteristics of chitosan, COS and its derivatives using fluorescently labeled forms of the compounds (fluorescein isothiocyanate/FITC-conjugated chitosan/COS).  

Absorption. Accumulated evidence from both in vitro and in vivo models indicates that COS is absorbed through the intestinal epithelia. COS can pass through a monolayer of Caco–2 cells, an in vitro model of absorptive intestinal epithelia, in a time and MW-dependent manner: as the MW of the COS decreases, the rate of absorption increases (Chae, et al., 2005). The rate of absorption of COS was higher than that of chitosan. Although low-MW chitosan (MWs of 13 kDa and 22 kDa) could be transported through Caco–2 monolayers, the high-MW COS (MW of 230 kDa) was non-absorbable. In addition, the cytotoxicity of COS to Caco–2 cells is inversely correlated to the MW of the COS and is lower than that of chitosan (Chae, et al., 2005; Zeng, et al., 2008). The ED50 values of COS (MW< 10 kDa) for inducing cytotoxicity in Caco–2 cells were > 20 mg/mL, while those of chitosan with MWs of 22 kDa and 230 kDa were 4.5 and 3.2 mg/mL, respectively (Chae, et al., 2005). In rats, a peak in the plasma concentration of COS was observed 30 min after oraladministration, which is later than that of chitosan. The rate of the in vivo intestinal absorption of COS was also inversely correlated to the MW of COS. Of note, the oral administration of COS (MW of 3.8kDa–7.5kDa) at 20mg/kg resulted in a peak plasma concentration of COS of 9 –20 g/mL. Consistent with the in vitro data, the chitosan with a MW of 230 kDa showed no intestinal absorption in rats (Chae, et al., 2005). These findings indicate that COS is able to be absorbed through intestinal epithelia.

Distribution. There have been several studies that investigated the tissue distribution of chitosan/COS and its derivatives including carboxymethyl and hydroxypropyl chitosan, which are water-soluble chitosan derivatives (Shao, et al., 2015). In most of the studies, FITC-chitosan/COS was given through the intraperitoneal or oral route. It has been demonstrated that chitosan/COS (~90%DD) was distributed mainly to the liver, spleen and kidneys (Dong, et al., 2010; Kean & Thanou, 2010). The highest level of chitosan/COS was found in the liver (Dong, et al., 2010; Zeng, et al., 2008). It has also been shown in some studies that lower portions of chitosan/COS were distributed to the heart and lung (Li, et al., 2015; Zeng, et al., 2008). Interestingly, the liver accumulation of low-MW COS (MW ~ 1 kDa) was less than that of chitosan (MW > 30 kDa) (Zeng, et al., 2008). In contrast, it has been reported that the decreased MW of chitosan (from 400 kDa to 100 kDa) was associated with a higher volume of distribution and the distribution of chitosan to the liver and kidneys (Dong, et al., 2012). These findings suggest that the MW ofchitosan/COS has an impact on their tissue distribution. Interestingly, the DD appears to affect the tissue distribution of chitosan/COS, as it has been found that chitosan with reduced DD (~50%) was accumulated in the kidneys more than in the liver and spleen (Onishi & Machida, 1999)

Metabolism. Both in vivo and in vitro experiments have demonstrated that chitosan/COS are degraded by lysozyme in the plasma, liver, kidney and urine (Onishi & Machida, 1999). After the administration of chitosan, a time-dependent reduction in the MW was observed (Dong, et al., 2010). A major proportion of the degraded product of chitosan is found in the liver, kidney and urine and has MW < 10 kDa (Li, et al., 2015). MW profiling of the chitosan degradation products in various tissues after the administration of high-MW chitosan (MW > 200 kDa) showed that the liver contained chitosan/COS with MWs ranging from < 1 kDa to 50 kDa (Shao, et al., 2015). In addition, the in vitro incubation of high-MW chitosan with liver lysates yielded degradation products with a mean MW of ~ 2.4 kDa. These findings suggest that the liver plays a central role in chitosan/COS biodegradation.  

Elimination. Kidneys play a key role in the excretion of chitosan/COS. Studies in rats showed that > 80% of the chitosan/COS is excreted in urine within 11 – 15 days after administration (Dong, et al., 2010; Dong, et al., 2012; Shao, et al., 2015). Interestingly, the MW of the chitosan/COS presented in the urine ranged from < 10 kDa to 40 kDa following the intraperitoneal administration of chitosan (MW ~ 300 kDa) (Dong, et al., 2010; Shao, et al., 2015). These results indicate that chitosan/COS is mainly eliminated in the urine after degradation in liver and kidney.


1. Chae, S. Y., Jang, M. K., & Nah, J. W. (2005). Influence of molecular weight on oral absorption of water soluble chitosans. J Control Release, 102, 383-394.

2. Li, H., Jiang, Z., Han, B., Niu, S., Dong, W., & Liu, W. (2015). Pharmacokinetics and biodegradation of chitosan in rats. J Ocean Univ China, 14, 897-904

3. Shao, K., Han, B., Dong, W., Song, F., Liu, W., & Liu, W. (2015). Pharmacokinetics and biodegradation performance of a hydroxypropyl chitosan derivative. J Ocean Univ China, 14, 888-896

4. Zeng, L., Qin, C., Wang, W., Chi, W., & Li, W. (2008). Absorption and distribution of chitosan in mice after oral administration.Carbohydr Polym, 71, 435-440.

5. Onishi, H., & Machida, Y. (1999). Biodegradation and distribution of water-soluble chitosan in mice. Biomaterials, 20, 175-182

6. Dong, W., Han, B., Feng, Y., Song, F., Chang, J., Jiang, H., et al. (2010). Pharmacokinetics and biodegradation mechanisms of a versatile carboxymethyl derivative of chitosan in rats: in vivo and in vitro evaluation. Biomacromolecules, 11, 1527-1533.

7. Kean, T., & Thanou, M. (2010). Biodegradation, biodistribution and toxicity of chitosan. Adv Drug Deliv Rev, 62, 3-11

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