1,2-Ethanediamine, N-(2-aminoethyl)-N'-[2-[(2-aminoethyl)amino]ethyl]-, reaction products with epichlorohydrin

281.83

281.1982382 g/mol

291-227-6

147003

C - Cardiovascular system

101 Ų

-2.206

1.091[at 20℃]

Insoluble

H412 (100%): Harmful to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]|P273, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

Overdosage with colestipol has not been reported. Regardless, in the case of overdosage, the chief potential harm would be obstruction of the gastrointestinal tract. The location of such potential obstruction, the degree of obstruction and the presence or absence of normal gut motility would determine treatment. No clinical data are available on the use of colestipol in pregnant women and during lactation. Colestipol does not appear to be absorbed systematically. Due to its known interference with absorption of fat-soluble vitamins, the use of colestipol in pregnancy or lactation or by women of childbearing potential requires that the benefits of drug therapy be weighed against the possible hazards to the mother and the child. There are no data on the effect of colestipol on fertility in humans. The use of colestipol in children is limited. Clinical trials conducted in children with colestipol ranules have usually employed doses of 5 to 20 g/day. The National Cholesterol Education Program (NCEP) Expert Panel recommends drug therapy be considered in children 10 years or older, who have previously undergone an adequate trial of diet therapy but still have unacceptably high serum cholesterol levels. In certain situations where a young child has extremely high serum cholesterol levels, drug treatment may even be initiated before 10 years of age. If the child is started on drug therapy, a carefully assessed diet therapy should also be continued in order to obtain optimal results. However, the safety of using colestipol tablets in patients under the age of 18 years has not been established. Furthermore, because bile acid sequestrants like colestipol may interfere with the absorption of fat-soluble vitamins, appropriate monitoring of growth and development is essential if colestipol is used in children. Appropriate studies on the relationship of age to the effects of colestipol have not been performed in the geriatric population. However, patients over 60 years of age may be more likely to experience gastrointestinal side effects, as well as adverse nutritional effects. Additionally, it has been determined that the oral LD50 in rats is > 1000 mg/kg [MSDS].

There is little evidence that colestipol causes liver injury. Mild elevations in serum aminotransferase and alkaline phosphatase levels have been reported in small numbers of patients on bile acid resins, although the elevations have been mild, transient and without accompanying symptoms. In addition, a case report of more marked aminotransferase elevations (>10 times ULN) with rapid recovery on stopping colestipol has been published, but the mechanism by which it might cause hepatotoxicity is very unclear. Colestipol is used in patients with liver disease to treat pruritus, and has little or no effect on serum enzyme or bilirubin levels.

Colestipol is not absorbed into the systemic circulation.

Colestipol is indicated as adjunctive therapy to diet for the reduction of elevated serum total and low-density lipoprotein cholesterol (LDL-C) in patients with primary hypercholesterolemia (a condition that features elevated LDL-C) who do not respond adequately to dietary changes . Therapy with lipid-altering agents like colestipol should be a component of multiple risk factor intervention in those individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Treatment should begin and continue with dietary therapy. In general, a minimum of six months of intensive dietary therapy and counseling should be carried out prior to initiation of drug therapy such as that with colestipol. Shorter periods may be considered in patients with severe elevations of LDL-C or with definite coronary heart disease. Although colestipol is effective in all types of hypercholesterolemia, some regional prescribing information note in particular that it is medically most appropriate in patients with Fredrickson's type II hyperlipoproteinemia. Nevertheless, in patients with combined hypercholesterolemia and hypertriglyceridemia, although colestipol may be helpful in reducing elevated cholesterol, it is not formally indicated where hypertriglyceridemia is the abnormality of greatest concern.|FDA Label

Colestipol is a nonabsorbed bile acid sequestrant that is used a therapy of hyperlipidemia and for the pruritus of chronic liver disease and biliary obstruction. Colestipol has not been associated with clinically apparent liver injury.

Antilipemic Agents

Cholesterol is the major, and probably the sole precursor of bile acids. During normal digestion, bile acids are secreted via the bile from the liver and gall bladder into the intestines. Bile acids emulsify the fat and lipid materials present in food, thus facilitating absorption. A major portion of the bile acids secreted is reabsorbed from the intestines and returned via the portal circulation to the liver, thus completing the enterohepatic cycle. Only very small amounts of bile acids are found in normal serum. Colestipol hydrochloride binds bile acids in the intestine forming a complex that is excreted in the feces. This nonsystemic action results in a partial removal of the bile acids from the enterohepatic circulation, preventing their reabsorption. Since colestipol hydrochloride is an anion exchange resin, the chloride anions of the resin can be replaced by other anions, usually those with a greater affinity for the resin than the chloride ion.

Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS. (See all compounds classified as Hypolipidemic Agents.)|High-molecular-weight insoluble polymers that contain functional cationic groups capable of undergoing exchange reactions with anions. (See all compounds classified as Anion Exchange Resins.)|Compounds that bind to and reduce the biological availability of a chemical or pharmaceutical agent. (See all compounds classified as Sequestering Agents.)

Colestipol is hydrophilic, but it is virtually water-insoluble (99.75%). This water insolubility, combined with the high molecular weight polymer in colestipol basically means the agent and the complexes it forms when it binds with bile acids are not absorbed. The action of colestipol is ultimately limited to the lumen of the gastrointestinal tract. It binds bile acids in the intestinal lumen and causes them to be excreted in the feces together with the polymer. When the enterohepatic circulation of bile acids is interrupted, cholesterol conversion to bile acids is enhanced and plasma cholesterol levels are thereby lowered.|Colestipol hydrochloride binds bile acids in the intestine forming a complex that is then ultimately excreted in the feces. In humans, less than 0.17% of a single 14C-labeled colestipol hydrochloride dose is excreted in the urine when given following 60 days of chronic dosing of 20 grams of colestipol hydrochloride per day. The increased fecal loss of bile acids due to colestipol hydrochloride administration leads to increased oxidation of cholesterol to bile acids.|Colestipol is not absorbed into the systemic circulation.

Colestipol is not absorbed into the systemic circulation nor is it hydrolyzed by any digestive enzymes.

Colestipol is not absorbed into the systemic circulation nor is it hydrolyzed by any digestive enzymes. Its action is ultimately limited to the lumen of the gastrointestinal tract, where it is eventually passed into the feces.

Colestipol is a lipid-lowering polymer that binds with bile acids in the intestine forming a complex that is excreted in the feces. This non-systemic action results in a continuous, partial removal of bile acids from the enterohepatic circulation preventing their reabsorption. This increased fecal loss of bile acids due to colestipol hydrochloride administration leads to increased oxidation of cholesterol to bile acids. This results in an increase in the number of hepatic low-density lipoprotein (LDL) receptors, and consequently an increased uptake of LDL and a decrease in serum/plasma beta lipoprotein or total and LDL cholesterol levels. Although hydrochloride produces an increase in the hepatic synthesis of cholesterol in man, serum cholesterol levels fall.

Colestid

1,2-Ethanediamine, N1-(2-aminoethyl)-N2-[2-[(2-aminoethyl)amino]ethyl]-, polymer with 2-(chloromethyl)oxirane: ACTIVE|XU - indicates a substance exempt from reporting under the Chemical Data Reporting Rule, (40 CFR 711).

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients