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Detail of "130167-69-0"

  • CAS Number:
  • 130167-69-0
  • Name:
  • Pegaspargase

  • Molecular Weight:
  • 0
  • Synonyms:
  • Oncaspar;Pegasparaginase

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CAS No.130167-69-0 Pegaspargase

pegaspargase p-INNList-64,1990;r-INNList-31,1991; asparaginase, reaction product with succinic anhydride, esters with polyethylene glycol monomethyl ether

Supplier:Tianjin Yaoyu Chemicals co.,ltd [ China (Mainland)]

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Reference

Pegaspargase: a review of clinical studies
Pegaspargase: a review of clinical studies. Graham, Michael L. (Department of Pediatrics, University of Arizona Health Sciences Center, Tucson, AZ 85724-5073, USA). Advanced Drug Delivery Reviews, 55(10), 1293-1302 (English) 2003 Elsevier Science B.V. CODEN: ADDREP. ISSN: 0169-409X. DOCUMENT TYPE: Journal; General Review CA Section: 1 (Pharmacology) Section cross-reference(s): 14 A review. The chemotherapy agent L-asparaginase has been an important part of acute lymphoblastic leukemia therapy for over 30 yr. 130167-69-0 and 9015-68-3 which are cas registry numbers are also used here. Two of the main disadvantages of the drug are (1) the need for frequent i.m. injection and (2) a very high rate of allergic reactions. Because of this, L-asparaginase seemed like an ideal target for pegylation and PEG-L-asparaginase was developed in the 1970s and 1980s. The drug has undergone extensive testing and appears to retain its antileukemic effectiveness while allowing less frequent administration than the native compd. While the actual cost to patients for PEG-L-asparaginase is greater than that of multiple injections of other L-asparaginases, the reduced need for physician visits and treatment of complications of therapy may make overall treatment costs considerably less than that of the conventional L-asparaginases. In the review below, the authors outline the history of therapy with L-asparaginase, the development of PEG-L-asparaginase, and clin. trials in which it has been administered. .
Asparaginase (native ASNase or pegylated ASNase) in the treatment of acute lymphoblastic leukemia
All Rights Reserved. Several substances are used for example 130167-69-0 and 9015-68-3 which are their cas registry numbers. Asparaginase (native ASNase or pegylated ASNase) in the treatment of acute lymphoblastic leukemia. Avramis, Vassilios I.; Tiwari, Prakash Nidhi (CHLA, Division of Hematology/Oncology, Department of Pediatrics, Keck School of Medicine, USC, Los Angeles, CA, USA). International Journal of Nanomedicine, 1(3), 241-254 (English) 2006 Dove Medical Press (NZ) Ltd. CODEN: IJNNHQ. ISSN: 1176-9114. DOCUMENT TYPE: Journal; General Review CA Section: 1 (Pharmacology) A review. The discovery of the tumor-inhibitory properties of asparaginase (ASNase) began in the early 1950s with the observation that guinea pig serum-treated lymphoma-bearing mice underwent rapid and often complete regression. About 4000 cases of acute lymphoblastic leukemia (ALL) are diagnosed very year in the US and many more through out the world. The majority of these cases are in children and young adults, making ALL the most common form of malignancy in these age groups. The treatment protocols of ALL are complex and use 6-12 drugs. Consequently, the improvement in the protocol design has improved significantly the success rate for long-term event-free survival in the past 20-30 years, which is now approx. 75% for patients afflicted with the higher risk ALL features and just above this percentage for patients with std. or good features. Despite this success, approx. 15% of patients die from ALL, making leukemic relapse the most common cause of treatment failure in pediatric oncol. ASNases have been the cornerstone of ALL therapies since the late 1970s. Native or pegylated L-asparaginase (ASNase or PEG-ASNase) are highly specific for the deamination of L-asparagine (Asn) to aspartic acid and ammonia. Depletion of Asn leads to a nutritional deprivation and inhibition of protein biosynthesis, resulting in apoptosis in T-lymphoblastic leukemias, which require Asn from external sources. The reactions of the host exposed to repeated ASNase treatments as well as the up-regulation of the mammalian enzymes to overcome the ASN-depletion toxic condition are of significant importance and may make us relearn the lessons on this important antileukemic drug. .
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