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HCID 214348Erstellt: 27. Oktober 2026

Deferasirox

Exjade · 20kg · 4-[3,5-bis(6-oxocyclohexa-2,4-dien-1-ylidene)-1,2,4-triazolidin-1-yl]benzoic acid · ICL-670 · Delarox · Delalox · CGP-72670 · Delazalim

https://huagongshe.com/de/chemical/214348

Molekülstruktur von Deferasirox

Identifikatoren & physikalische Daten

CAS No.201530-41-8
SummenformelC21H15N3O4
Durchschnittliche Molmasse373,4 g/mol
Monoisotopische Masse373,10625596 g/mol
SMILESO=C(O)c1ccc(-n2nc(-c3ccccc3O)nc2-c2ccccc2O)cc1
InChIKeyBOFQWVMAQOTZIW-UHFFFAOYSA-N
PubChem CID214348
ChEMBLCHEMBL550348
ChEBICHEBI:49005
EC No.685-491-5
DTXSIDDTXSID1048596

Chemische & physikalische Eigenschaften

XLogP3,8
Polarare Oberfläche (TPSA)108
H-Brücken-Donoren3
H-Brücken-Akzeptoren6
Frei drehbare Bindungen4
Schwere Atome28
Formalladung0
Komplexität540
ArzneimittelPharmaceuticals -> Listed in ZINC15
LogP (Verteilungskoeffizient)log Kow = 6.30 (pH 7.4)3.52
Color/FormCrystals from ethanolWhite to slightly yellow powder
LöslichkeitIn water, 0.4 mg/mL at 25 °C (pH 7.40)3.43e-02 g/LSoluble in DMSO (10 mg/ml)
Human DrugsBreast FeedingLactationMilk, HumanChelating AgentsIron Chelating AgentsFDA approved drugs -> Active ingredientEMA approved medicines: Human medicine
Schmelzpunkt116-117 °C264-265 °C116 - 117 °C260-2620C
Physical DescriptionSolid
Dissociation ConstantspKa1 = 4.57pKa2 = 8.71pKa3 = 10.56Dissociation constant also reported in H2O/DMSO (X(DMSO = 0.20) as pKa1 = 4.61pKa2 = 10.12pKa3 = 12.08
Siedepunkt672.1±65.0 °C(Predicted)
Dichte1.40±0.1 g/cm3(Predicted)
LagerbedingungenKeep in dark place,Inert atmosphere,2-8°C
pKa (Säurekonstante)pKa1 4.57, pKa2 8.71, pKa3 10.56 (Nick)Also reported in H2O/DMSO (CDMSO = 0.20) as pKa1 4.61, pKa2 10.12, pKa3 12.08 (Steinhauser)
Aggregatzustandsolid
FarbeOff-white to white
StabilitätStable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 1 month.
InChIInChI=1S/C21H15N3O4/c25-17-7-3-1-5-15(17)19-22-20(16-6-2-4-8-18(16)26)24(23-19)14-11-9-13(10-12-14)21(27)28/h1-12,25-26H,(H,27,28)
InChIKeyBOFQWVMAQOTZIW-UHFFFAOYSA-N
SMILESC(O)(=O)C1=CC=C(N2C(C3=CC=CC=C3O)=NC(C3=CC=CC=C3O)=N2)C=C1

Sicherheit & Vorschriften

GHS-EinstufungThis chemical does not meet GHS hazard criteria for 9.1% (1 of 11) of reports.WarningH302 (54.5%): Harmful if swallowed [Warning Acute toxicity, oral]P261, P264, P264+P265, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P317, P319, P321, P330, P332+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 11 reports by companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
FDA-AnforderungenThe Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including deferasirox, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.
Hazard Classes and CategoriesAcute Tox. 4 (54.5%)
EntsorgungsverfahrenSRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.
WechselwirkungenConcomitant use of UGT inducers or cholestyramine decreases deferasirox systemic exposure (AUC). Avoid the concomitant use of cholestyramine or potent UGT inducers (eg, rifampicin, phenytoin, phenobarbital, ritonavir) with Exjade. If you must co-administer these agents together, consider increasing the initial dose of Exjade to 30 mg/kg, and monitor serum ferritin levels and clinical responses for further dose modification.The concomitant administration of Exjade and aluminum-containing antacid preparations has not been formally studied. Although deferasirox has a lower affinity for aluminum than for iron, do not administer Exjade with aluminum-containing antacid preparations.

Anwendungen & Verwendung

Beschreibung

Linagliptin was originally discovered at Boehringer Ingelheim as an orally active dipeptidyl peptidase-IV (DPP-4) inhibitor. Eli Lilly and Boehringer Ingelheim co-developed and launched linagliptin for type II diabetes as an adjunct to diet and exercise for the improvement of adult glycemic control. Linagliptin has a superior DPP-4 IC50 value of 1 nM, compared with 19 nM for sitagliptin, 24 nM for alogliptin, 50 nM for saxagliptin and 62 nM for vildagliptin. In addition, linagliptin exhibited prolonged pharmacodynamic activity with long-lasting DPP-4 inhibition in several preclinical species. Linagliptin showed good efficacy in phase II clinical trials with doses as low as 5 mg and no signs of hypoglycemia with doses as high as 600 mg. The prolonged pharmacological effect of DPP-4 activity and the good safety/tolerability profile provided the basis for linagliptin’s approval.

Verwenden

Biological Activity Chemical Information Tech Support & FAQs Biological Activity Deferasirox(Exjade) is a rationally-designed oral iron chelator. Its main use is to reduce chronic iron overload in patients who are receiving long-term blood transfusions

HepatotoxicityIn large clinical trials of deferasirox, elevations in serum aminotransferase levels above 5 times the upper limit of normal (ULN) occurred in 6% of patients and led to drug discontinuation in 1% to 2%. In addition, there have been several single case reports of clinically apparent liver injury arising during deferasirox therapy which was often severe and occasionally fatal. The onset of acute liver injury ranged from a few days to severak years after starting deferasirox but most cases occurred within 1 to 3 months. The pattern of liver injury was typically hepatocellular or mixed with prominent elevations in serum aminotransferase levels. Immunoallergic and autoimmune features were absent. Recovery was usually rapid once deferasirox was stopped, but some cases were associated with progressive liver injury and hepatic failure. Because patients with iron overload often have underlying liver disease, a superimposed acute hepatocellular injury may result in an increased risk of acute liver failure. Deferasirox has a boxed warning regarding hepatotoxicity and regular monitoring of serum bilirubin and aminotransferase levels is recommended.
Human Toxicity Excerpts/HUMAN EXPOSURE STUDIES/ This study was designed to investigate the effect of deferasirox on the QT/QTc interval. A randomized, single-dose, placebo- and positive-controlled, parallel-group study was conducted in a total of 182 healthy subjects. Study participants were randomized to four treatments arms: deferasirox 20 mg/kg (n = 46), deferasirox 40 mg/kg (n = 46), placebo (n = 46) or moxifloxacin 400 mg (n = 44). Moxifloxacin tablets were taken in an open-label fashion, while the subjects and investigator staff remained blinded for the other treatments. Electrocardiograms, obtained at various time points during a 24-hr period, were evaluated centrally in a blinded fashion. The primary endpoint was the average change from baseline in QT/QTc over the 24-hr period following intake of study medication. It was prospectively defined that deferasirox will be considered devoid of inducing QT/QTc-prolongation if the upper bound of the 95% 2-sided confidence interval (CI) for the difference to placebo is below 8 milliseconds (ie, being noninferior to placebo). Deferasirox 20 and 40 mg/kg were noninferior to placebo with respect to the average change from baseline in QT/QTc, as indicated by 95% CIs for the mean treatment difference (deferasirox 20 or 40 mg/kg minus placebo), which were entirely below 8 milliseconds. The lower limit of the 95% 2-sided CI for the difference between moxifloxacin and placebo was greater than 0 milliseconds, demonstrating the sensitivity of the study. Deferasirox C(max) and AUC following intake of deferasirox 40 mg/kg was higher by factor 1.6 and 2.3, respectively, than observed at a steady state in beta-thalassemia patients treated for 6 months with deferasirox 30 mg/kg, the recommended maximum dose. This study demonstrates that deferasirox does not prolong the QT/QTc interval at both therapeutic and supratherapeutic plasma concentrations. It is, therefore, not expected that deferasirox has a negative effect on cardiac repolarization in patients under treatment with this medication./SIGNS AND SYMPTOMS/ Cases of overdose (2-3 times the prescribed dose for several weeks) have been reported. In one case, this resulted in hepatitis which resolved without long-term consequences after a dose interruption. Single doses up to 80 mg/kg/day in iron overloaded beta-thalassemic patients have been tolerated with nausea and diarrhea noted. In healthy volunteers, single doses of up to 40 mg/kg/day were tolerated./CASE REPORTS/ In this report /the authors/ present a 37-year-old thalassemia patient with hyperferritinemia referred to /a/ Microcytemia Center at the beginning of deferasirox (DFX) therapy. Treatment with subcutaneous infusions of desferrioxamine (DFO) had started when he was 10 years old. During the 6-month DFX treatment, serum ferritin levels progressively increased from 600 to 2,700 ng/mL despite progressive DFX dose adjustments.This paradoxically abnormal ferritin levels required drug discontinuation but were not paralleled by a similar iron burden in T2 * magnetic resonance imaging. In this clinical case, ferritin levels were inappropriately increased following initiation of DFX treatment, but in the presence of an almost unmodified pattern of organ iron overload. Excluding the diagnostic dilemma of an improbable failure of DFX chelation, the pathogenesis of this phenomenon remains to be clarified .../CASE REPORTS/ ... This report describes the hepatotoxicity induced by Deferasirox in a patient with haemochromatosis with a discussion of possible pathogenetic mechanism.For more Human Toxicity Excerpts (Complete) data for Deferasirox (14 total), please visit the HSDB record page.
Drug Induced Liver InjuryDrug Induced Liver Injury Rank (DILIrank 2.0)DeferasiroxvMost-DILI-concern7Box warningDOI:10.1016/j.drudis.2016.02.015
Non-Human Toxicity Excerpts/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ /The authors/ investigated whether deferasirox is capable of removing cardiac iron and improving iron-induced pathogenesis of the heart using the iron overload gerbil model. Animals were randomly divided into three groups: control, iron overload, and iron overload + deferasirox treatment. Iron-dextran was given 100 mg/kg per 5 days i.p for 10 weeks. Deferasirox treatment was taken post iron loading and was given at 100 mg/kg/day p.o for 1 or 3 months. Cardiac iron concentration was determined by inductively coupled plasma atomic emission spectroscopy. Compared with the untreated group, deferasirox treatment for 1 and 3 months decreased cardiac iron concentration 17.1% (P = 0.159) and 23.5% (P < 0.05), respectively. These treatment-associated reductions in cardiac iron were paralleled by decreases in tissue ferritin expression of 20% and 38% at 1 and 3 months, respectively (P < 0.05). Using oxyblot analysis and hydroethidine fluorescence, we showed that deferasirox significantly reduces cardiac protein oxidation and superoxide abundance by 36 and 47.1%, respectively (P < 0.05). .../LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A 26-week oral carcinogenicity study in p53 (+/-) transgenic mice has shown no evidence of carcinogenicity from deferasirox at doses up to 200 mg/kg per day in males and 300 mg/kg per day in females./LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A 104-week oral carcinogenicity study in Wistar rats showed no evidence of carcinogenicity from deferasirox at doses up to 60 mg/kg per day./LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Deferasirox at oral doses up to 75 mg/kg per day was found to have no adverse effect on fertility and reproductive performance of male and female rats.For more Non-Human Toxicity Excerpts (Complete) data for Deferasirox (6 total), please visit the HSDB record page.
Antidote and Emergency Treatment/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B//SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B//SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/
Effects During Pregnancy and Lactation◉ Summary of Use during Lactation
Wassergefährdungsklasse (WGK)WGK 3
Zollcode2933997500
Lagerklasse11 - Combustible Solids
Gefahrstoffdaten201530-41-8(Hazardous Substances Data)
GefahrenklasseAcute Tox. 4 OralAquatic Acute 1