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1. 1,3-bis(2-chloroethyl)-1-nitrosourea
2. Bcnu
3. Bicnu
4. Fivb
5. N,n'-bis(2-chloroethyl)-n-nitrosourea
6. Nitrumon
1. 154-93-8
2. 1,3-bis(2-chloroethyl)-1-nitrosourea
3. Bcnu
4. Gliadel
5. Carmubris
6. Carmustin
7. Nitrumon
8. Bicnu
9. Becenun
10. Bischloroethyl Nitrosourea
11. Bi Cnu
12. Carmustinum
13. 1,3-bis(2-chloroethyl)nitrosourea
14. Bischlorethylnitrosurea
15. N,n'-bis(2-chloroethyl)-n-nitrosourea
16. Bischlorethylnitrosourea
17. Carmustina
18. Urea, N,n'-bis(2-chloroethyl)-n-nitroso-
19. Nsc-409962
20. Bis(2-chloroethyl)nitrosourea
21. Fda 0345
22. Sri 1720
23. Bicnu (tn)
24. Dti 015
25. Nci-c04773
26. Sk 27702
27. Carmustine (98%)
28. Bis(chloroethyl)nitrosourea
29. Nsc 409962
30. Bis-chloroethylnitrosourea
31. Nsc409962
32. Chembl513
33. 1,3-bis(2-chloroethyl)-1-nitroso-urea
34. Chebi:3423
35. Urea, 1,3-bis(2-chloroethyl)-1-nitroso-
36. Becenum
37. Dti-015
38. U68wg3173y
39. Fda-0345
40. Sri-1720
41. 1,3-bis(2-chloroethyl)-3-nitrosourea
42. Ncgc00015204-05
43. Sk-27702
44. 1,3-bis(.beta.-chloroethyl)-1-nitrosourea
45. Gliadel Wafer
46. Bischloroethylnitrosourea
47. Dsstox_cid_2743
48. Dsstox_rid_76712
49. Carmustinum [inn-latin]
50. Dsstox_gsid_22743
51. Carmustina [inn-spanish]
52. Bis(2-chloroethyl)1-nitrosourea
53. Bis-n,n'-(chloroethyl)nitrosourea
54. Cas-154-93-8
55. Ccris 810
56. 1,3-bis(beta-chloroethyl)-1-nitrosourea
57. Bcnu [chloroethyl Nitrosoureas]
58. Sr-01000075736
59. Einecs 205-838-2
60. Brn 2049744
61. Camustine
62. Carustine
63. Unii-u68wg3173y
64. Ai3-52216
65. Hsdb 7761
66. Bicnu; Nitrumon
67. Carmustine [usan:usp:inn:ban]
68. Carmustine- Bio-x
69. Prestwick_997
70. Gliadel (tn)
71. Bischloroethyl Nitrosourea [chloroethyl Nitrosoureas]
72. Mfcd00057706
73. Gliadel (mgi Pharm)
74. Spectrum_000265
75. Carmustine, >=98%
76. Carmustine [mi]
77. Carmustine [inn]
78. Carmustine [jan]
79. Spectrum4_000888
80. Spectrum5_000920
81. Camustine [vandf]
82. Carmustine [hsdb]
83. Carmustine [usan]
84. Lopac-c-0400
85. Wln: Onn2gvm2g
86. C 0400
87. Carmustine [mart.]
88. Schembl4503
89. Carmustine [usp-rs]
90. Carmustine [who-dd]
91. Lopac0_000188
92. Carmustine (jan/usp/inn)
93. Kbiogr_001296
94. Kbioss_000745
95. Mls001333962
96. Divk1c_000835
97. Amy382
98. Gtpl6800
99. Carmustine [ep Impurity]
100. Carmustine [orange Book]
101. Dtxsid8022743
102. Hms502j17
103. Kbio1_000835
104. Kbio2_000745
105. Kbio2_003313
106. Kbio2_005881
107. Carmustine [ep Monograph]
108. Ninds_000835
109. Carmustine [usp Monograph]
110. Hms2092j22
111. Hms2230i05
112. Hms3260f17
113. Hms3369d17
114. Pharmakon1600-01503110
115. Bcp27690
116. Zinc3830387
117. Tox21_110097
118. Tox21_500188
119. Bdbm50015950
120. Ccg-39925
121. Nsc758392
122. Stk624770
123. Akos005558013
124. Tox21_110097_1
125. Bcp9000490
126. Db00262
127. Lp00188
128. Nsc-758392
129. Sdccgsbi-0050176.p004
130. Idi1_000835
131. Urea,3-bis(2-chloroethyl)-1-nitroso-
132. Bischloroethyl Nitrosourea [iarc]
133. Ncgc00015204-01
134. Ncgc00015204-02
135. Ncgc00015204-03
136. Ncgc00015204-04
137. Ncgc00015204-06
138. Ncgc00015204-07
139. Ncgc00015204-08
140. Ncgc00015204-09
141. Ncgc00015204-18
142. Ncgc00093665-01
143. Ncgc00093665-02
144. Ncgc00093665-03
145. Ncgc00093665-04
146. Ncgc00260873-01
147. Urea,n'-bis(2-chloroethyl)-n-nitroso-
148. Ac-24196
149. As-12106
150. Bc164289
151. Hy-13585
152. N,n''-bis(2-chloroethyl)-n-nitrosourea
153. Nci60_003931
154. Smr000058426
155. Sbi-0050176.p003
156. Eu-0100188
157. Ft-0602937
158. S3669
159. Bcnu; 1,3-bis(2-chloroethyl)-1-nitrosourea
160. C06873
161. D00254
162. Ab00052431-07
163. Ab00052431_08
164. 154c938
165. A809590
166. Q415869
167. Sr-01000075736-1
168. Sr-01000075736-3
169. W-108025
170. Z1563145982
171. Carmustine, United States Pharmacopeia (usp) Reference Standard
172. 1-(2-chloroethyl)-1-([(2-chloroethyl)amino]carbonyl)-2-oxohydrazine #
| Molecular Weight | 214.05 g/mol |
|---|---|
| Molecular Formula | C5H9Cl2N3O2 |
| XLogP3 | 1.5 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 4 |
| Exact Mass | 213.0071819 g/mol |
| Monoisotopic Mass | 213.0071819 g/mol |
| Topological Polar Surface Area | 61.8 Ų |
| Heavy Atom Count | 12 |
| Formal Charge | 0 |
| Complexity | 156 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 4 | |
|---|---|
| Drug Name | Bicnu |
| PubMed Health | Carmustine |
| Drug Classes | Antineoplastic Agent |
| Active Ingredient | Carmustine |
| Dosage Form | Injectable |
| Route | Injection |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Emcure Pharms |
| 2 of 4 | |
|---|---|
| Drug Name | Gliadel |
| PubMed Health | Carmustine |
| Drug Classes | Antineoplastic Agent |
| Active Ingredient | Carmustine |
| Dosage Form | Implant |
| Route | Intracranial |
| Strength | 7.7mg |
| Market Status | Prescription |
| Company | Arbor Pharms |
| 3 of 4 | |
|---|---|
| Drug Name | Bicnu |
| PubMed Health | Carmustine |
| Drug Classes | Antineoplastic Agent |
| Active Ingredient | Carmustine |
| Dosage Form | Injectable |
| Route | Injection |
| Strength | 100mg/vial |
| Market Status | Prescription |
| Company | Emcure Pharms |
| 4 of 4 | |
|---|---|
| Drug Name | Gliadel |
| PubMed Health | Carmustine |
| Drug Classes | Antineoplastic Agent |
| Active Ingredient | Carmustine |
| Dosage Form | Implant |
| Route | Intracranial |
| Strength | 7.7mg |
| Market Status | Prescription |
| Company | Arbor Pharms |
BiCNU is indicated as palliative therapy as a single agent or in established combination therapy with other approved chemotherapeutic agents in the following: Brain tumors-glioblastoma, brainstem glioma, medulloblastoma, astrocytoma, ependymoma, and metastatic brain tumors. Multiple myeloma-in combination with prednisone. Hodgkin's Disease-as secondary therapy in combination with other approved drugs in patients who relapse while being treated with primary therapy, or who fail to respond to primary therapy. Non-Hodgkin's lymphomas-as secondary therapy in combination with other approved drugs for patients who relapse while being treated with primary therapy, or who fail to respond to primary therapy.
US Natl Inst Health; DailyMed. Current Medication Information for BiCNU (carmustine) (October 2007). Available from, as of November 9, 2009: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=5694
bis(Chloroethyl) nitrosourea has been used since 1971 as an antineoplastic agent in the treatment of Hodgkin's lymphoma, multiple myeloma, and primary or metastatic brain tumors.
DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Carmustine (bis(Chloroethyl) nitrosourea) (154-93-8) (January 2005). Available from, as of September 18, 2009: https://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s037bcnu.pdf
Reported to have antiviral, antibacterial, and antifungal activity, but no evidence was found that it is currently used for these purposes. Former use.
DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Carmustine (bis(Chloroethyl) nitrosourea) (154-93-8) (January 2005). Available from, as of September 29, 2009: https://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s037bcnu.pdf
MEDICATION (VET): A chemotherapeutic protocol using carmustine in combination with vincristine and prednisone was tested in dogs with multicentric malignant lymphosarcoma. Of seven dogs treated, six (85.7%) achieved complete remission. A partial response occurred in one dog. Median survival time was 224 days (mean 386 days), and median duration of remission was 183 days (mean 323 days). Marked neutropenia was observed following carmustine administration. There were no significant alterations in platelets and red blood cell counts during treatment, and no abnormalities attributable to the chemotherapy were found in serum biochemical profiles. Results of this study showed that carmustine is an effective alternative option in the treatment of canine lymphosarcoma.
PMID:15238559 Ricci Lucas SR et al; J Am Anim Hosp Assoc 40 (4): 292-9 (2004)
/BOXED WARNING/ WARNING: BiCNU (carmustine for injection) should be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. Bone marrow suppression, notably thrombocytopenia and leukopenia, which may contribute to bleeding and overwhelming infections in an already compromised patient, is the most common and severe of the toxic effects of BiCNU. Since the major toxicity is delayed bone marrow suppression, blood counts should be monitored weekly for at least 6 weeks after a dose. At the recommended dosage, courses of BiCNU should not be given more frequently than every 6 weeks. The bone marrow toxicity of BiCNU is cumulative and therefore dosage adjustment must be considered on the basis of nadir blood counts from prior dose. Pulmonary toxicity from BiCNU appears to be dose related. Patients receiving greater than 1400 mg/sq m cumulative dose are at significantly higher risk than those receiving less. Delayed pulmonary toxicity can occur years after treatment, and can result in death, particularly in patients treated in childhood.
US Natl Inst Health; DailyMed. Current Medication Information for BiCNU (carmustine) (Updated: June 2014). Available from, as of April 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=be6776fe-7f24-417d-ef08-8830c4eca959
Human systemic effects by parenteral, intravenous, and possibly other routes: nausea or vomiting, reduced white blood cell and blood platelet counts, bone marrow damage, and potentially fatal respiratory system effects, including lung fibrosis, dyspnea, and cyanosis.
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 466
In a study of 17 children (aged 1-16 years) receiving carmustine in cumulative doses ranging from 770-1800 mg/sq m combined with cranial radiation therapy for intracranial tumors, 8 children (47%) died of delayed pulmonary fibrosis, including all of those who received initial treatment at less than 5 years of age (5 children). Onset of pulmonary fibrosis has been observed up to 17 years following carmustine therapy. Clinical findings include pulmonary hypoplasia with upper zone contraction on chest radiographs, and an unusual pattern of upper zone fibrosis on thoracic CT scans; no abnormal findings were observed on gallium scans.105 Late onset of reduction in pulmonary function was observed in all long-term survivors in the study. Carmustine-induced pulmonary fibrosis may be slowly progressive and cause death.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 981
Pulmonary toxicity, including acute or delayed onset of pulmonary fibrosis causing death, has occurred in patients receiving systemic carmustine therapy. Pulmonary toxicity characterized by pulmonary infiltrates and/or fibrosis occurring 9 days to 43 months following treatment has been reported in patients receiving carmustine or related nitrosoureas. Most reported cases of pulmonary toxicity have occurred in patients receiving prolonged carmustine therapy with total doses exceeding 1400 mg/sq m; however, pulmonary fibrosis has occurred with lower total doses. Other risk factors include prior history of pulmonary disease and duration of carmustine therapy. Pulmonary toxicity occasionally has been rapidly progressive and/or fatal.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 980-1
For more Drug Warnings (Complete) data for Carmustine (41 total), please visit the HSDB record page.
For the treatment of brain tumors, multiple myeloma, Hodgkin's disease and Non-Hodgkin's lymphomas.
FDA Label
Carmustine is effective in the following malignant neoplasms as a single agent or in combination with other antineoplastic agents and/or other therapeutic measures (radiotherapy, surgery):
- Brain tumours (glioblastoma, brain-stem gliomas, medulloblastoma, astrocytoma and ependymoma), brain metastases
- Secondary therapy in non-Hodgkins lymphoma and Hodgkins disease
- as conditioning treatment prior to autologous haematopoietic progenitor cell transplantation (HPCT) in malignant haematological diseases (Hodgkins disease / Non-hodgkins lymphoma).
Carmustine is one of the nitrosoureas indicated as palliative therapy as a single agent or in established combination therapy with other approved chemotherapeutic agents in treatment of brain tumors, multiple myeloma, Hodgkin's disease, and non-Hodgkin's lymphomas. Although it is generally agreed that carmustine alkylates DNA and RNA, it is not cross resistant with other alkylators. As with other nitrosoureas, it may also inhibit several key enzymatic processes by carbamoylation of amino acids in proteins.
Antineoplastic Agents, Alkylating
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026) (See all compounds classified as Antineoplastic Agents, Alkylating.)
L01AD01
L - Antineoplastic and immunomodulating agents
L01 - Antineoplastic agents
L01A - Alkylating agents
L01AD - Nitrosoureas
L01AD01 - Carmustine
Absorption
5 to 28% bioavailability
Route of Elimination
Approximately 60% to 70% of a total dose is excreted in the urine in 96 hours and about 10% as respiratory CO2.
Following IV infusion of carmustine, the steady-state volume of distribution averaged 3.25 L/kg. Because of their high lipid solubility, carmustine and/or its metabolites readily cross the blood-brain barrier. Substantial CSF concentrations occur almost immediately after IV administration of carmustine, and CSF concentrations of radioactivity have been variously reported to range from 15-70% of concurrent plasma concentrations. Carmustine metabolites are distributed into milk, but in concentrations less than those in maternal plasma.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 983
The absorption of the copolymer contained in carmustine wafers has not been evaluated in humans. Plasma concentrations of carmustine following intracranial implantation of the wafers have not been determined in humans, but in rabbits undergoing surgical implantation of wafers containing 3.85% carmustine, no detectable levels of carmustine were observed in plasma.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 983
When the carmustine wafer is exposed to the aqueous environment of the resection cavity, hydrolysis of the anhydride bonds in the copolymer occurs, resulting in the release of carmustine and two monomers, carboxyphenoxypropane, and sebacic acid. The carmustine contained in the wafer diffuses into the surrounding brain tissue. The metabolism and excretion of the copolymer contained in carmustine wafers has not been evaluated in humans. Animal studies have shown that more than 70% of the copolymer degrades within 3 weeks following implantation of carmustine wafers into brain tissue; following hydrolysis of the copolymer, carboxyphenoxypropane is eliminated renally, while sebacic acid (an endogenous fatty acid) is metabolized in the liver and expired as carbon dioxide. In humans, wafer remnants have been observed on brain imaging scans or located during subsequent surgical procedures up to 8 months following intracranial implantation. Wafer remnants retrieved from 2 patients approximately 2-3 months after implantation were analyzed and found to consist mostly of water and monomeric components with minimal detectable amounts of carmustine.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 983
The disappearance of 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU) from plasma, liver, kidney, lung, brain, spleen, tumor tissue and epididymal adipose tissue of Walker 256/B carcinoma-bearing rats and healthy animals was measured by differential pulse polarography after i.v. bolus of the drug. Only BCNU, not its decomposition products, was detected by the polarographic assay. Levels of BCNU in liver of tumor-bearing animals were significantly lower (about 10 times) than those on healthy rats. A bi-exponential fit was used to calculate the kinetics of BCNU in plasma, kidney, lung and brain, but no difference could be found between healthy and Walker tumor-bearing rats. BCNU disappeared faster from adipose tissue of tumor-bearing animals than from normals.
PMID:6531791 Bartosek I et al; Tumori 70 (6): 491-8 (1984).
Some 40 minutes after injection, BCNU is no longer an effective antitumour agent, and a few minutes after administration no unchanged BCNU can be detected in plasma. Following its ip or sc injection or oral administration, BCNU was rapidly distributed to most tissues, including brain and cerebrospinal fluid. Excretion was primarily in the urine; it was most rapid in mice (80% of the dose excreted in 24 hours) and less rapid in monkeys and dogs.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V26 85 (1981)
Hepatic and rapid with active metabolites. Metabolites may persist in the plasma for several days.
The in vitro metabolism of the anticancer agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) has been studied in male Fischer 344 rat liver microsomal preparations. The previously identified product, 1,3-bis(2-chloroethyl)urea (BCU), has been shown to be the major metabolite. Stable isotope labeling and mass spectral analysis of isolated metabolites indicate that BCU is formed exclusively from the metabolic denitrosation of BCNU. The rate of BCNU chemical decomposition in rat liver microsomal preparations deficient in NADPH and the metabolic disappearance rate in preparations containing added NADPH were measured and compared with the measured rate of metabolic formation of BCU under the same conditions. The rate of NADPH-dependent BCNU metabolism and BCU formation are equal within experimental error. BCNU was found to inhibit the rat liver 9000 g supernatant metabolism of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU).
PMID:7252986 Lin HS, Weinkam RJ; J Med Chem 24 (6): 761-3 (1981).
15-30 minutes
Carmustine causes cross-links in DNA and RNA, leading to the inhibition of DNA synthesis, RNA production and RNA translation (protein synthesis). Carmustine also binds to and modifies (carbamoylates) glutathione reductase. This leads to cell death.
Temozolomide (TMZ) and carmustine (BCNU), cancer-drugs usually used in the treatment of gliomas, are DNA-methylating agents producing O6-methylguanine. It has been shown that 06-methylguanine triggers DNA mismatch repair and in turn induce apoptosis and senescence, respectively, over a 4 and 6 days period. Temozolomide and carmustine have an earlier effect on nuclear organization and chromatin structure. In particular, temozolomideZ and carmustine induce clustering of pericentromeric heterochromatin regions and increase the amount of heterochromatic proteins MeCP2 and HP1alpha bound to chromatin. These drugs also decrease global levels of histone H3 acetylation and increase levels of histone H3 trimethylated on lysine 9 (H3-triMeK9). These events precede the senescence status. ... Temozolomide and carmustine efficacy in glioma treatment may implicate a first event characterized by changes in heterochromatin organization and its silencing which is then followed by apoptosis and senescence.
PMID:19116135 Papait R et al; Biochem Biophys Res Commun 379 (2): 434-9 (2009).
Although carmustine is believed to act by alkylation of DNA and RNA, the mechanism of action has not been completely elucidated and other effects such as carbamoylation and modification of cellular proteins may be involved. The overall result is thought to be the inhibition of both DNA and RNA synthesis.
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 983
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