コンドロイチン硫酸

This chemical does not meet GHS hazard criteria for 63.6% (7 of 11) of all reports.

Danger

H317 (36.4%): May cause an allergic skin reaction [Warning Sensitization, Skin]

P233, P260, P261, P271, P272, P280, P284, P302+P352, P304+P340, P317, P321, P333+P317, P342+P316, P362+P364, P403, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 11 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Chondroitin, hydrogen sulfate

XU - indicates a substance exempt from reporting under the Chemical Data Reporting Rule, (40 CFR 711).

Chondroitin, hydrogen sulfate, sodium salt: Does not have an individual approval but may be used under an appropriate group standard

Chondroitin hydrogen sulfate: Does not have an individual approval but may be used under an appropriate group standard

M - Musculo-skeletal system

QM - Musculo-skeletal system

In clinical trials, chondroitin sulfate has been reported a significant pain relief. Some reports have shown no slow in joint damage. The effects of chondroitin sulfate have been very controversial. One of the characteristics of chondroitin is a slow onset of action with a maximal effect attained after several months. Chondroitin sulfate has been reported to have anti-inflammatory properties by reducing the synovitis and prevent proinflammatory cytokine up-regulation in arthritis models. It is also registered an anabolic effect of chondroitin sulfate in which it induces the synthesis of hyaluronate in synovial cells, it increases type II collagen and proteoglycan synthesis.

Chondroitin sulfate functions as a major component of the intricate extracellular matrix. It is proposed that chondroitin sulfate supply can provide new building blocks for the synthesis of new matrix components. The anti-inflammatory effect of chondroitin sulfate is thought to be caused by the inhibition of the synthesis of inflammatory intermediates such as the inhibition of nitric oxide synthase, COX-2, microsomal prostaglandin synthase 1 and prostaglandin E2. It is reported also an inhibitory activity in the toll-like receptor 4 which will later inhibit inflammatory cytokines, NFkB and MyD88. This activity suggests a modulation of the MAP kinase pathway. On the other hand, some reports have pointed out an induction on the PKC/PI3K/Akt pathway in neuroblastoma. The anabolic effect of chondroitin sulfate is suggested to be caused by the inhibition of metalloproteinases such as MMP-1, -3 and -13 as well as ADAMTS-4 and -5.

The approximate half-life of chondroitin sulfate and its derivative metabolites is 15 hours. After intramuscular administration of chondroitin sulfate in humans, the elimination half-life of the chondroitin sulfate was of 275 min. When administered orally, the elimination half-life was presented at 310 min.

Chondroitin sulfate is not metabolized by cytochrome P450. Reports have indicated the presence in plasma of mono-, oligo- and polysaccharides with a molecular weight of less of 5 kDa which are derived from the partial digestion of exogenous chondroitin sulfate. The reported degradation of chondroitin sulfate seems to be very complex and led by the formation of smaller digestion derivatives of the original form.

Chondroitin sulfate is absorbed from the gastrointestinal tract. The absorbed portion reaches a ratio of 10% as unchanged chondroitin sulfate and 90% as depolymerized low-molecular-weight derivatives. This absorption depends on the sulfation status. The bioavailability of chondroitin sulfate ranges from 10-20% following oral administration. Reports have shown a consistent accumulation of the compound in joint tissue. The steady-state is attained after 3-4 days and it takes around 3-6 months to obtain the maximal effect. After intramuscular administration of chondroitin sulfate, the peak plasma level of 3.8 mcg/ml was reached after 90 min. When given orally, the peak plasma concentration of 4.6 mcg/ml was reached after 240 min.

Chondroitin sulfate is excreted in the urine as intact polymers and as partial degradation products. After intramuscular administration, about 37% of the administered dose is excreted by urine during the first 24 hours as high- and low-molecular-weight derivatives.

After intramuscular administration of chondroitin sulfate, the apparent volume of distribution was 0.40 ml/g. When administered orally, the apparent volume of distribution changed to 0.44ml/g.