Floxuridine 50-91-9 Antineoplastic Drugs Raw Powder High Purity

Basic Information
Place of Origin: CHINA
Brand Name: TINGYI
Certification: GMP , ISO 9001:2008
Model Number: 50-91-9
Minimum Order Quantity: 10g
Price: Contact Me
Packaging Details: Disguised Package
Delivery Time: 2 Working Days
Payment Terms: Bank Transfer - Bitcoin - Western Union - MoneyGram
Supply Ability: 100 KG/Month
Product Name: Floxuridine CAS: 50-91-9
Synonym: FUDR Usage: Muscle Gaining
Shipping Method: EMS, HKEMS, FEDEX, DHL, UPS, Aramex, ETC Color: White
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Quick Information 

Product Name Floxuridine
CAS 50-91-9
Purity 99%
MW 246.19
MS Floxuridine 50-91-9 Antineoplastic Drugs Raw Powder High Purity 0



Floxuridine (FUDR) is a pyrimidine analogue used as an antineoplastic agent, usually as a continuous hepatic arterial infusion to treat hepatic metastases from colon cancer. Intraarterial floxuridine is associated with a very high rate of serum enzyme and bilirubin elevations during therapy, and with frequent biliary damage that can result in a secondary sclerosing cholangitis, which can be severe and lead to cirrhosis.



Floxuridine (flox ure' i deen) is a fluoropyrimidine (fluorodeoxyuridine; FUDR) that has antineoplastic action against several solid tumors including liver, gastrointestinal adenocarcinoma and colorectal cancers. Floxuridine, like fluorouracil, requires conversion to monophosphate and possibly the triphosphate. It appears to act by inhibition of production or direct competition with thymidine triphosphate, which is necessary for DNA synthesis. Floxuridine was approved for use as an anticancer agent in the United States in 1970 and is given predominantly by continuous infusion into the hepatic artery to treat metastatic carcinoma of the colon or following resection of colon cancer metastases.


Floxuridine is available as a powder for reconstitution in 500 mg vials (5 mL, 100 mg/mL) in several generic forms. Floxuridine is typically given by infusion pump into the hepatic artery in a dose of 0.1 to 0.6 mg/kg/day. Because the liver metabolizes floxuridine, administration by direct infusion into the hepatic artery deceases the systemic side effects which can be severe. Common side effects of intraarterial therapy include bone marrow suppression, fatigue, weakness, headache, dizziness, insomnia, paresthesias, abdominal pain, constipation, diarrhea, dyspepsia, nausea, stomatitis, and rash.




Serum aminotransferase elevations occur in a high proportion of patients given floxuridine by infusion into the hepatic artery, the reported rates ranging from 25% to 100%. These elevations are generally mild to moderate in severity and resolve with stopping therapy. "Chemical hepatitis," however, not infrequently is a cause of dose modification or delay in cycles of treatment. In addition, prolonged or repeated hepatic arterial infusions of FUDR can cause acalculous cholecystitis and multiple biliary strictures that can cause jaundice and a chronic sclerosing cholangitis-like syndrome. Between 5% and 25% of patients treated with hepatic arterial infusions of FUDR will develop symptomatic biliary strictures with pain and jaundice. These typically arise after 2 to 6 months of therapy, but can appear later, even more than a year after initiating FUDR therapy.


The biliary strictures typically affect central bile ducts in the area of the porta hepatis, generally in and around the bifurcation of the common hepatic duct. Similar inflammation and fibrosis account for the acalculous cholecystitis that can occur with FUDR therapy, but which can be avoided by cholecystectomy at the time of hepatic resection of metastases or placement of the intraarterial infusion pump. The biliary strictures generally improve with stopping therapy, but can progress or require endoscopic or surgical intervention. Deaths from progressive biliary strictures and cholestatic liver injury have been described and can be a major cause of death among survivors of this metastatic tumor. The frequency of biliary strictures after FUDR therapy may be decreased by concurrent administration of dexamethasone and avoided by monitoring with hepatic and biliary imaging. However, the many complications of hepatic arterial infusion chemotherapy have decreased enthusiasm for this therapy, particularly with newer, more potent systemic antineoplastic agents.



Mechanism of Injury

FUDR can cause both hepatocellular (chemical hepatitis) and cholestatic (biliary strictures, cholangitis) injury. Both appear to be the direct, intrinsic toxicity of FUDR. In a dog animal model, the biliary injury can be reproduced with hepatic artery infusions and the hepatocellular injury (without bile duct damage) by portal vein infusions of FUDR.


Outcome and Management

The severity of the liver injury linked to floxuridine therapy ranges from minimal and transient serum enzyme elevations to severe cholestatic liver injury due to severe biliary strictures. Hepatic injury arising during FUDR therapy is a frequent reason for dose modification or delay in cycles of therapy. Appearance of jaundice due to hepatic arterial infusions of FUDR should lead to its discontinuation, as further therapy usually worsens the course. If the infusions are discontinued early, partial recovery with resolution of jaundice and symptoms is not uncommon. There is little evidence for cross sensitivity to hepatic injury among the various pyrimidine analogue antineoplastic agents. However, hepatic toxicity between floxuridine and fluorouracil can be additive.


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