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Furosemide
Also known as: 54-31-9, Frusemide, Lasix, Furosemid, Furanthril, Errolon
Molecular Formula
C12H11ClN2O5S
Molecular Weight
330.74  g/mol
InChI Key
ZZUFCTLCJUWOSV-UHFFFAOYSA-N
FDA UNII
7LXU5N7ZO5

A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
Furosemide is a Loop Diuretic. The physiologic effect of furosemide is by means of Increased Diuresis at Loop of Henle.
1 2D Structure

Furosemide

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
4-chloro-2-(furan-2-ylmethylamino)-5-sulfamoylbenzoic acid
2.1.2 InChI
InChI=1S/C12H11ClN2O5S/c13-9-5-10(15-6-7-2-1-3-20-7)8(12(16)17)4-11(9)21(14,18)19/h1-5,15H,6H2,(H,16,17)(H2,14,18,19)
2.1.3 InChI Key
ZZUFCTLCJUWOSV-UHFFFAOYSA-N
2.1.4 Canonical SMILES
C1=COC(=C1)CNC2=CC(=C(C=C2C(=O)O)S(=O)(=O)N)Cl
2.2 Other Identifiers
2.2.1 UNII
7LXU5N7ZO5
2.3 Synonyms
2.3.1 MeSH Synonyms

1. Errolon

2. Frusemid

3. Frusemide

4. Furanthril

5. Furantral

6. Furosemide Monohydrochloride

7. Furosemide Monosodium Salt

8. Fursemide

9. Fusid

10. Lasix

2.3.2 Depositor-Supplied Synonyms

1. 54-31-9

2. Frusemide

3. Lasix

4. Furosemid

5. Furanthril

6. Errolon

7. Fusid

8. Aisemide

9. Beronald

10. Desdemin

11. Frusemin

12. Fuluvamide

13. Furanthryl

14. Furantril

15. Fursemide

16. Lowpstron

17. Macasirool

18. Prefemin

19. Rosemide

20. Trofurit

21. Fulsix

22. Furesis

23. Katlex

24. Lasilix

25. Radonna

26. Seguril

27. Transit

28. Lasex

29. Salix

30. Urex

31. Marsemide

32. Eutensin

33. Frusetic

34. Fursemid

35. Logirene

36. Oedemex

37. Promedes

38. Frusid

39. Lazix

40. Mirfat

41. Frusemid

42. Frusenex

43. Furanturil

44. Furosedon

45. Profemin

46. Urosemide

47. Aluzine

48. Diural

49. Dryptal

50. Impugan

51. Nicorol

52. Rusyde

53. Uremide

54. Uresix

55. Yidoli

56. Disal

57. Laxur

58. Urian

59. Apo-frusemide

60. Hydro-rapid

61. Anfuramaide

62. Arasemide

63. Bioretic

64. Disemide

65. Diurapid

66. Diurolasa

67. Diusemide

68. Durafurid

69. Fluidrol

70. Frusedan

71. Fuluvamine

72. Furobeta

73. Furodiurol

74. Furodrix

75. Furorese

76. Furosemidum

77. Furosemix

78. Furoside

79. Furosifar

80. Furovite

81. Fursemida

82. Hissuflux

83. Hydroled

84. Jenafusid

85. Lasiletten

86. Lowpston

87. Moilarorin

88. Novosemide

89. Protargen

90. Radisemide

91. Selectofur

92. Sigasalur

93. Spirofur

94. Synephron

95. Zafimida

96. Aldalix

97. Aquarid

98. Aquasin

99. Cetasix

100. Dirine

101. Discoid

102. Diurin

103. Diusil

104. Diuzol

105. Dranex

106. Edemid

107. Edenol

108. Endural

109. Farsix

110. Franyl

111. Frumex

112. Frumide

113. Frusema

114. Furetic

115. Furfan

116. Furmid

117. Furocot

118. Furomen

119. Furomex

120. Furosan

121. Furose

122. Furosix

123. Furoter

124. Fursol

125. Hydrex

126. Kofuzon

127. Kolkin

128. Kutrix

129. Lasemid

130. Liside

131. Luscek

132. Nelsix

133. Odemase

134. Odemex

135. Promide

136. Puresis

137. Radouna

138. Salinex

139. Salurex

140. Salurid

141. Uridon

142. Uritol

143. Aldic

144. Depix

145. Desal

146. Eliur

147. Fluss

148. Furex

149. Furix

150. Golan

151. Hydro

152. Nadis

153. Retep

154. Rosis

155. Vesix

156. Mita

157. Apo-furosemide

158. Furo-puren

159. Lasix Retard

160. Polysquall A

161. 4-chloro-n-furfuryl-5-sulfamoylanthranilic Acid

162. Less Diur

163. Neo-renal

164. Furo-basan

165. Furosemidu

166. Urex-m

167. Nephron

168. Furomide M.d.

169. Furosemida

170. 4-chloro-n-(2-furylmethyl)-5-sulfamoylanthranilic Acid

171. Lb 502

172. 5-(aminosulfonyl)-4-chloro-2-[(2-furylmethyl)amino]benzoic Acid

173. 2-furfurylamino-4-chloro-5-sulfamoylbenzoic Acid

174. Lb-502

175. Nci-c55936

176. Lasix (tn)

177. Benzoic Acid, 5-(aminosulfonyl)-4-chloro-2-[(2-furanylmethyl)amino]-

178. 4-chloro-2-[(furan-2-ylmethyl)amino]-5-sulfamoylbenzoic Acid

179. Diumide-k

180. 4-chloro-5-sulfamoyl-n-furfuryl-anthranilic Acid

181. 4-chloro-2-(furan-2-ylmethylamino)-5-sulfamoylbenzoic Acid

182. Chlor-n-(2-furylmethyl)-5-sulfamylanthranilsaeure

183. Anthranilic Acid, 4-chloro-n-furfuryl-5-sulfamoyl-

184. Chembl35

185. 4-chloro-2-((furan-2-ylmethyl)amino)-5-sulfamoylbenzoic Acid

186. Nsc-269420

187. Benzoic Acid, 5-(aminosulfonyl)-4-chloro-2-((2-furanylmethyl)amino)-

188. 7lxu5n7zo5

189. Chebi:47426

190. Furosemidu [polish]

191. 5-(aminosulfonyl)-4-chloro-2-((2-furanylmethyl)amino)benzoic Acid

192. 5-(aminosulfonyl)-4-chloro-2-[(2-furanylmethyl)amino]benzoic Acid

193. Cas-54-31-9

194. Furosemidum [inn-latin]

195. Furosemida [inn-spanish]

196. Ncgc00016241-06

197. Sal Diureticum

198. 4-chloro-2-{[(furan-2-yl)methyl]amino}-5-sulfamoylbenzoic Acid

199. Dsstox_cid_648

200. Dsstox_rid_75710

201. Dsstox_gsid_20648

202. Furosemide "mita"

203. Fun

204. Furosemide Mita

205. Furosemide Oral

206. 5-(aminosulfonyl)-4-chloro-2-([2-furanylmethyl]amino)benzoic Acid

207. 5-(aminosulfonyl)-4-chloro-2-[(furan-2-ylmethyl)amino]benzoic Acid

208. Smr000058202

209. Ccris 1951

210. Furosemide ''mita''

211. Hsdb 3086

212. Sr-01000765380

213. Einecs 200-203-6

214. Hoe-058a

215. Unii-7lxu5n7zo5

216. Nsc 269420

217. Brn 0840915

218. Neosemid

219. Zafurida

220. Chlor-n-(2-furylmethyl)-5-sulfamylanthranilsaeure [german]

221. 5-(aminosulfonyl)-4-chloro-2-((2-furylmethyl)amino)benzoic Acid

222. Furosemide, 4

223. Urex M

224. Furosemide (lasix)

225. Prestwick_752

226. Frumil (salt/mix)

227. Mfcd00010549

228. Furosemide [usan:usp:inn:ban:jan]

229. Spectrum_001100

230. 1z9y

231. 4-chloro-2-[(2-furylmethyl)amino]-5-sulfamoylbenzoic Acid

232. Furosemide [mi]

233. Furosemide [inn]

234. Furosemide [jan]

235. Prestwick0_000341

236. Prestwick1_000341

237. Prestwick2_000341

238. Prestwick3_000341

239. Spectrum2_001005

240. Spectrum3_000437

241. Spectrum4_000560

242. Spectrum5_000744

243. Furosemide [hsdb]

244. Furosemide [iarc]

245. Furosemide [usan]

246. F0182

247. Furosemide [vandf]

248. Upcmld-dp022

249. Furosemide [mart.]

250. Schembl9811

251. Furosemide [usp-rs]

252. Furosemide [who-dd]

253. Furosemide [who-ip]

254. Oprea1_667724

255. Bspbio_000401

256. Bspbio_002054

257. Kbiogr_001259

258. Kbioss_001580

259. 5-18-09-00555 (beilstein Handbook Reference)

260. Mls001066374

261. Mls001306403

262. Mls002548896

263. Bidd:gt0139

264. Divk1c_000575

265. Spectrum1500310

266. Spbio_001129

267. Spbio_002322

268. Bpbio1_000443

269. Furosemide (jp17/usp/inn)

270. Gtpl4839

271. Furosemide [green Book]

272. Dtxsid6020648

273. Furosemide [orange Book]

274. Upcmld-dp022:001

275. Bdbm25902

276. Hms501m17

277. Kbio1_000575

278. Kbio2_001580

279. Kbio2_004148

280. Kbio2_006716

281. Kbio3_001274

282. Zinc35804

283. 4-chloro-2-(2-furylmethylamino)-5-sulfamoyl-benzoic Acid

284. Furosemide [ep Monograph]

285. Ninds_000575

286. Furosemide [usp Monograph]

287. Hms1569e03

288. Hms1920b03

289. Hms2090k06

290. Hms2091h05

291. Hms2096e03

292. Hms2233h03

293. Hms3259m03

294. Hms3370j22

295. Hms3655e09

296. Hms3713e03

297. Hms3874g03

298. Pharmakon1600-01500310

299. Furosemide 1.0 Mg/ml In Methanol

300. Furosemidum [who-ip Latin]

301. Albb-019200

302. Hy-b0135

303. Tox21_110322

304. Tox21_202213

305. Tox21_302971

306. Bbl027780

307. Ccg-40223

308. Nsc269420

309. Nsc757039

310. Stk177334

311. Wln: T5oj B1mr Cg Fvq Dszw

312. Akos000266625

313. Furosemide 100 Microg/ml In Methanol

314. Tox21_110322_1

315. Bcp9000708

316. Cs-1915

317. Db00695

318. Ks-1226

319. Nc00453

320. Nsc-757039

321. Idi1_000575

322. Smp1_000129

323. Ncgc00016241-01

324. Ncgc00016241-02

325. Ncgc00016241-03

326. Ncgc00016241-04

327. Ncgc00016241-05

328. Ncgc00016241-07

329. Ncgc00016241-08

330. Ncgc00016241-10

331. Ncgc00016241-11

332. Ncgc00090893-01

333. Ncgc00090893-02

334. Ncgc00090893-03

335. Ncgc00090893-05

336. Ncgc00090893-06

337. Ncgc00256523-01

338. Ncgc00259762-01

339. Ac-11067

340. Bf166384

341. Bp-13261

342. Sbi-0051389.p003

343. Db-052536

344. Ab00052001

345. Sw196894-3

346. 54f319

347. C07017

348. D00331

349. D87719

350. Ab00052001-10

351. Ab00052001-11

352. Ab00052001_12

353. Ab00052001_13

354. A830094

355. Q388801

356. Sr-01000765380-2

357. Sr-01000765380-3

358. Sr-01000765380-7

359. Brd-k78010432-001-05-8

360. Brd-k78010432-001-10-8

361. Z275128584

362. 4-chloro-2-(2-furanylmethylamino)-5-sulfamoylbenzoic Acid

363. Furosemide, British Pharmacopoeia (bp) Reference Standard

364. Furosemide, European Pharmacopoeia (ep) Reference Standard

365. 4-chloranyl-2-(furan-2-ylmethylamino)-5-sulfamoyl-benzoic Acid

366. Furosemide, United States Pharmacopeia (usp) Reference Standard

367. 4-chloro-n-furfuryl-5-sulfamoylanthranilic Acid Furosemide

368. 4-chloro-n-furfuryl-5-sulfamoylanthranilic Acid??furosemide

369. 5-(aminosulfamyl)-4-chloro-2-[(2-furanylmethyl)amino]benzoic Acid

370. 5-(aminosulfonyl)-4-chloro-2-[(2-furylmethyl)amino]benzoic Acid #

371. 4-chloro-n-furfuryl-5-sulfamoylanthranilic Acid Pound>>furosemide

372. Furosemide, Pharmaceutical Secondary Standard; Certified Reference Material

373. Furosemide For Peak Identification, European Pharmacopoeia (ep) Reference Standard

374. Furosemide Solution, 1.0 Mg/ml In Methanol, Ampule Of 1 Ml, Certified Reference Material

2.4 Create Date
2005-03-25
3 Chemical and Physical Properties
Molecular Weight 330.74 g/mol
Molecular Formula C12H11ClN2O5S
XLogP32
Hydrogen Bond Donor Count3
Hydrogen Bond Acceptor Count7
Rotatable Bond Count5
Exact Mass330.0077203 g/mol
Monoisotopic Mass330.0077203 g/mol
Topological Polar Surface Area131 Ų
Heavy Atom Count21
Formal Charge0
Complexity481
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Drug Information
1 of 6  
Drug NameFurosemide
PubMed HealthFurosemide
Drug ClassesCardiovascular Agent
Drug LabelThe CAS Registry Number is 54-31-9.It has a molecular formula of C12H11ClN2O5S and a molecular weight of 330.75.The molecular structure is as follows:...
Active IngredientFurosemide
Dosage FormTablet; Injectable; Solution
RouteInjection; Oral
Strength40mg/5ml; 10mg/ml; 80mg; 40mg; 20mg
Market StatusPrescription
CompanyVintage Pharms; Wockhardt; Excellium; Hospira; Sun Pharm Inds; Sandoz; Roxane; Ivax Sub Teva Pharms; Emcure Pharms; Fresenius Kabi Usa; Ipca Labs; Claris Lifesciences; Luitpold; Mylan

2 of 6  
Drug NameLasix
PubMed HealthFurosemide
Drug ClassesCardiovascular Agent
Drug LabelLASIX is a diuretic which is an anthranilic acid derivative. LASIX tablets for oral administration contain furosemide as the active ingredient and the following inactive ingredients: lactose monohydrate NF, magnesium stearate NF, starch NF, talc US...
Active IngredientFurosemide
Dosage FormTablet
RouteOral
Strength80mg; 40mg; 20mg
Market StatusPrescription
CompanySanofi Aventis Us

3 of 6  
Drug NameUrex
Active IngredientMethenamine hippurate
Dosage FormTablet
RouteOral
Strength1gm
Market StatusPrescription
CompanyCnty Line Pharms

4 of 6  
Drug NameFurosemide
PubMed HealthFurosemide
Drug ClassesCardiovascular Agent
Drug LabelThe CAS Registry Number is 54-31-9.It has a molecular formula of C12H11ClN2O5S and a molecular weight of 330.75.The molecular structure is as follows:...
Active IngredientFurosemide
Dosage FormTablet; Injectable; Solution
RouteInjection; Oral
Strength40mg/5ml; 10mg/ml; 80mg; 40mg; 20mg
Market StatusPrescription
CompanyVintage Pharms; Wockhardt; Excellium; Hospira; Sun Pharm Inds; Sandoz; Roxane; Ivax Sub Teva Pharms; Emcure Pharms; Fresenius Kabi Usa; Ipca Labs; Claris Lifesciences; Luitpold; Mylan

5 of 6  
Drug NameLasix
PubMed HealthFurosemide
Drug ClassesCardiovascular Agent
Drug LabelLASIX is a diuretic which is an anthranilic acid derivative. LASIX tablets for oral administration contain furosemide as the active ingredient and the following inactive ingredients: lactose monohydrate NF, magnesium stearate NF, starch NF, talc US...
Active IngredientFurosemide
Dosage FormTablet
RouteOral
Strength80mg; 40mg; 20mg
Market StatusPrescription
CompanySanofi Aventis Us

6 of 6  
Drug NameUrex
Active IngredientMethenamine hippurate
Dosage FormTablet
RouteOral
Strength1gm
Market StatusPrescription
CompanyCnty Line Pharms

4.2 Therapeutic Uses

Diuretics; Sodium Potassium Chloride Symporter Inhibitors

National Library of Medicine's Medical Subject Headings. Furosemide. Online file (MeSH, 2017). Available from, as of April 10, 2017: https://www.nlm.nih.gov/mesh/2017/mesh_browser/MBrowser.html


Oral Lasix may be used in adults for the treatment of hypertension alone or in combination with other antihypertensive agents. Hypertensive patients who cannot be adequately controlled with thiazides will probably also not be adequately controlled with Lasix alone. /Included in US product labeling/

NIH; DailyMed. Current Medication Information for Lasix (Furosemide Tablet) (Updated: April 2016). Available from, as of April 19, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2c9b4d8f-0770-482d-a9e6-9c616a440b1a


Lasix is indicated in adults and pediatric patients for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. Lasix is particularly useful when an agent with greater diuretic potential is desired. /Included in US product labeling/

NIH; DailyMed. Current Medication Information for Lasix (Furosemide Tablet) (Updated: April 2016). Available from, as of April 19, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2c9b4d8f-0770-482d-a9e6-9c616a440b1a


IV furosemide has been found useful as an adjunct to hypotensive agents in the treatment of hypertensive crises, especially when associated with acute pulmonary edema or renal failure. In addition to producing a rapid diuresis, furosemide enhances the effects of other hypotensive drugs and counteracts the sodium retention caused by some of these agents. /NOT included in US product labeling/

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2828


For more Therapeutic Uses (Complete) data for Furosemide (11 total), please visit the HSDB record page.


4.3 Drug Warning

/BOXED WARNING/ Lasix (furosemide) is a potent diuretic which, if given in excessive amounts, can lead to a profound diuresis with water and electrolyte depletion. Therefore, careful medical supervision is required and dose and dose schedule must be adjusted to the individual patient's needs.

NIH; DailyMed. Current Medication Information for Lasix (Furosemide Tablet) (Updated: April 2016). Available from, as of April 19, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2c9b4d8f-0770-482d-a9e6-9c616a440b1a


Excessive diuresis may cause dehydration and blood volume reduction with circulatory collapse and possibly vascular thrombosis and embolism, particularly in elderly patients. As with any effective diuretic, electrolyte depletion may occur during Lasix therapy, especially in patients receiving higher doses and a restricted salt intake. Hypokalemia may develop with Lasix, especially with brisk diuresis, inadequate oral electrolyte intake, when cirrhosis is present, or during concomitant use of corticosteroids, ACTH, licorice in large amounts, or prolonged use of laxatives. Digitalis therapy may exaggerate metabolic effects of hypokalemia, especially myocardial effects.

NIH; DailyMed. Current Medication Information for Lasix (Furosemide Tablet) (Updated: April 2016). Available from, as of April 19, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2c9b4d8f-0770-482d-a9e6-9c616a440b1a


Patients receiving furosemide must be carefully observed for signs of hypovolemia, hyponatremia, hypokalemia, hypocalcemia, hypochloremia, and hypomagnesemia. Patients should be informed of the signs and symptoms of electrolyte imbalance and instructed to report to their physicians if weakness, dizziness, fatigue, faintness, mental confusion, lassitude, muscle cramps, headache, paresthesia, thirst, anorexia, nausea, and/or vomiting occur. Excessive fluid and electrolyte loss may be minimized by initiating therapy with small doses, careful dosage adjustment, using an intermittent dosage schedule if possible, and monitoring the patient's weight. To prevent hyponatremia and hypochloremia, intake of sodium may be liberalized in most patients; however, patients with cirrhosis usually require at least moderate sodium restriction while on diuretic therapy. Determinations of serum electrolytes, BUN, and carbon dioxide should be performed early in therapy with furosemide and periodically thereafter. If excessive diuresis and/or electrolyte abnormalities occur, the drug should be withdrawn or dosage reduced until homeostasis is restored. Electrolyte abnormalities should be corrected by appropriate measures.

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2830


Furosemide should be used with caution in patients with hepatic cirrhosis because rapid alterations in fluid and electrolyte balance may precipitate hepatic precoma or coma.

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2830


For more Drug Warnings (Complete) data for Furosemide (29 total), please visit the HSDB record page.


4.4 Drug Indication

Furosemide is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, in adults and pediatric patients. Oral furosemide is indicated alone for the management of mild to moderate hypertension or severe hypertension in combination with other antihypertensive medications. Intravenous furosemide is indicated as adjunctive therapy in acute pulmonary edema when a rapid onset of diuresis is desired.


Treatment of fluid retention


5 Pharmacology and Biochemistry
5.1 Pharmacology

Furosemide manages hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome. Furosemide is a potent loop diuretic that works to increase the excretion of Na+ and water by the kidneys by inhibiting their reabsorption from the proximal and distal tubules, as well as the loop of Henle. It works directly acts on the cells of the nephron and indirectly modifies the content of the renal filtrate. Ultimately, furosemide increases the urine output by the kidney. Protein-bound furosemide is delivered to its site of action in the kidneys and secreted via active secretion by nonspecific organic transporters expressed at the luminal site of action. Following oral administration, the onset of the diuretic effect is about 1 and 1.5 hours, and the peak effect is reached within the first 2 hours. The duration of effect following oral administration is about 4-6 hours but may last up to 8 hours. Following intravenous administration, the onset of effect is within 5 minutes, and the peak effect is reached within 30 minutes. The duration of action following intravenous administration is approximately 2 hours. Following intramuscular administration, the onset of action is somewhat delayed.


5.2 MeSH Pharmacological Classification

Sodium Potassium Chloride Symporter Inhibitors

Agents that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS which are concentrated in the thick ascending limb at the junction of the LOOP OF HENLE and KIDNEY TUBULES, DISTAL. They act as DIURETICS. Excess use is associated with HYPOKALEMIA and HYPERGLYCEMIA. (See all compounds classified as Sodium Potassium Chloride Symporter Inhibitors.)


Diuretics

Agents that promote the excretion of urine through their effects on kidney function. (See all compounds classified as Diuretics.)


5.3 FDA Pharmacological Classification
5.3.1 Active Moiety
FUROSEMIDE
5.3.2 FDA UNII
7LXU5N7ZO5
5.3.3 Pharmacological Classes
Loop Diuretic [EPC]; Increased Diuresis at Loop of Henle [PE]
5.4 ATC Code

C03CA01

S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355


C - Cardiovascular system

C03 - Diuretics

C03C - High-ceiling diuretics

C03CA - Sulfonamides, plain

C03CA01 - Furosemide


5.5 Absorption, Distribution and Excretion

Absorption

Following oral administration, furosemide is absorbed from the gastrointestinal tract. It displays variable bioavailability from oral dosage forms, ranging from 10 to 90%. The oral bioavailability of furosemide from oral tablets or oral solution is about 64% and 60%, respectively, of that from an intravenous injection of the drug.


Route of Elimination

The kidneys are responsible for 85% of total furosemide total clearance, where about 43% of the drug undergoes renal excretion. Significantly more furosemide is excreted in urine following the I.V. injection than after the tablet or oral solution. Approximately 50% of the furosemide load is excreted unchanged in urine, and the rest is metabolized into glucuronide in the kidney.


Volume of Distribution

The volume of distribution following intravenous administration of 40 mg furosemide were 0.181 L/kg in healthy subjects and 0.140 L/kg in patients with heart failure.


Clearance

Following intravenous administration of 400 mg furosemide, the plasma clearance was 1.23 mL/kg/min in patients with heart failure and 2.34 mL/kg/min in healthy subjects, respectively.


Significantly more furosemide is excreted in urine following the IV injection than after the tablet or oral solution. There are no significant differences between the two oral formulations in the amount of unchanged drug excreted in urine.

NIH; DailyMed. Current Medication Information for Lasix (Furosemide Tablet) (Updated: April 2016). Available from, as of April 19, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=2c9b4d8f-0770-482d-a9e6-9c616a440b1a


After oral administration of furosemide to 18 pregnant women on the day of delivery, substantial concentrations of the drug were detected in umbilical cord vein plasma as well as in amniotic fluid. The ratio between the furosemide concentrations in maternal vein plasma and in umbilical cord plasma increased with time and approximated unity at 8 to 10 hr after administration of the drug. The plasma half-life of furosemide appeared to be longer in the mothers than in nonpregnant healthy volunteers. In one patient the plasma level of furosemide was constant during 5 hr of observation.

PMID:699480 Beermann B et al; Clin Pharmacol Ther 24 (5): 560-2 (1978)


In one study in patients with normal renal function, approx 60% of a single 80 mg oral dose of furosemide was absorbed from the GI tract. When admin to fasting adults in this dosage, the drug appeared in the serum within 10 min, reached a peak concn of 2.3 ug/mL in 60-70 min, & was almost completely cleared from the serum in 4 hr. When the same dose was given after a meal, the serum concn of furosemide increased slowly to a peak of about 1 ug/ml after 2 hr & similar concns were present 4 hr after ingestion. However, a similar diuretic response occurred regardless of whether the drug was given with food or to fasting patients. In another study, the rate & extent of absorption varied considerably when 1 g of furosemide was given orally to uremic patients. An avg of 76% of a dose was absorbed, & peak plasma concns were achieved within 2-9 hr (avg 4.4 hr). Serum concns required to produce max diuresis are not known, & it has been reported that the magnitude of response does not correlate with either the peak or the mean serum concns.

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2831


The diuretic effect of orally administered furosemide is apparent within 30 minutes to 1 hr and is maximal in the first or second hour. The duration of action is usually 6-8 hr. The maximum hypotensive effect may not be apparent until several days after furosemide therapy is begun. After iv administration of furosemide, diuresis occurs within 5 min, reaches a maximum within 20-60 min, and persists for approximately 2 hr. After im administration, peak plasma concentrations are attained within 30 min; onset of diuresis occurs somewhat later than after iv administration. In patients with severely impaired renal function, the diuretic response may be prolonged.

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2831


For more Absorption, Distribution and Excretion (Complete) data for Furosemide (15 total), please visit the HSDB record page.


5.6 Metabolism/Metabolites

The metabolism of furosemide occurs mainly in the kidneys and the liver, to a smaller extent. The kidneys are responsible for about 85% of total furosemide total clearance, where about 40% involves biotransformation. Two major metabolites of furosemide are furosemide glucuronide, which is pharmacologically active, and saluamine (CSA) or 4-chloro-5-sulfamoylanthranilic acid.


It would appear that frusemide glucuronide is the only or at least the major biotransformation metabolite in man. 2-amino-4- chloro-5-sulfamoylanthranilic acid has been reported in some studies but not in others; and is thought to be an analytical artifact.

International Programme on Chemical Safety (IPCS); Poisons Information Monograph (PIM) No. 240, Furosemide (July 1997). Available from, as of April 18, 2017: https://www.inchem.org/pages/pims.html


In patients with normal renal function, a small amount of furosemide is metabolized in the liver to the defurfurylated derivative, 4-chloro-5-sulfamoylanthranilic acid. ...

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2831


5.7 Biological Half-Life

The half-life from the dose of 40 mg furosemide was 4 hours following oral administration and 4.5 hours following intravenous administration. The terminal half-life of furosemide is approximately 2 hours following parenteral administration. The terminal half-life may be increased up to 24 hours in patients with severe renal failure.


To study the pharmacokinetics of furosemide (fursemide; Lasix) and its acyl glucuronide and to analyze the pharmacodynamic response, a study was conducted in 7 healthy subjects, mean age 34 yr, who received a single oral 80 mg dose of furosemide in tablet form. Two half-lives were distinguished in the plasma elimination of furosemide and its conjugate, with values of 1.25 and 30.4 hr for furosemide and 1.31 and 33.2 hr for the conjugate. ...

Vree TB et al; J Pharm Pharmacol (Nov): 964-9 (1995)


In dogs, ... the elimination half life /is/ approximately 1-1.5 hours.

Plumb D.C. Veterinary Drug Handbook. 8th ed. (pocket). Ames, IA: Wiley-Blackwell, 2015., p. 644


Various investigators have reported a wide range of elimination half-lives for furosemide. In one study, the elimination half-life averaged about 30 minutes in healthy patients who received 20-120 mg of the drug IV. In another study, the elimination half-life averaged 9.7 hours in patients with advanced renal failure who received 1 g of furosemide IV. The elimination half-life was more prolonged in 1 patient with concomitant liver disease.

American Society of Health-System Pharmacists 2016; Drug Information 2016. Bethesda, MD. 2016, p. 2831


The serum half-life in therapeutic doses is 92 minutes; increasing in patients with uremia; congestive heart failure and cirrhosis as well as in the neonate and aged patients. In such patients the half-life may be extended to 20 hours.

International Programme on Chemical Safety (IPCS); Poisons Information Monograph (PIM) No. 240, Furosemide (July 1997). Available from, as of April 18, 2017: https://www.inchem.org/pages/pims.html


5.8 Mechanism of Action

Furosemide promotes diuresis by blocking tubular reabsorption of sodium and chloride in the proximal and distal tubules, as well as in the thick ascending loop of Henle. This diuretic effect is achieved through the competitive inhibition of sodium-potassium-chloride cotransporters (NKCC2) expressed along these tubules in the nephron, preventing the transport of sodium ions from the lumenal side into the basolateral side for reabsorption. This inhibition results in increased excretion of water along with sodium, chloride, magnesium, calcium, hydrogen, and potassium ions. As with other loop diuretics, furosemide decreases the excretion of uric acid. Furosemide exerts direct vasodilatory effects, which results in its therapeutic effectiveness in the treatment of acute pulmonary edema. Vasodilation leads to reduced responsiveness to vasoconstrictors, such as angiotensin II and noradrenaline, and decreased production of endogenous natriuretic hormones with vasoconstricting properties. It also leads to increased production of prostaglandins with vasodilating properties. Furosemide may also open potassium channels in resistance arteries. The main mechanism of action of furosemide is independent of its inhibitory effect on carbonic anhydrase and aldosterone.


Though both in vivo and in vitro studies have demonstrated an anticonvulsant effect of the loop diuretic furosemide, the precise mechanism behind this effect is still debated. The current study investigates the effect of furosemide on Cs-induced epileptiform activity (Cs-FP) evoked in area CA1 of rat hippocampal slices in the presence of Cs(+) (5mM) and ionotropic glutamatergic and GABAergic receptor antagonists. As this model diverges in several respects from other epilepsy models it can offer new insight into the mechanism behind the anticonvulsive effect of furosemide. The present study shows that furosemide suppresses the Cs-FP in a dose-dependent manner with a near complete block at concentrations = 1.25 mM. Because furosemide targets several types of ion transporters we examined the effect of more selective antagonists. Bumetanide (20 uM), which selectively inhibits the Na-K-2Cl co-transporter (NKCC1), had no significant effect on the Cs-FP. VU0240551 (10 uM), a selective antagonist of the K-Cl co-transporter (KCC2), reduced the ictal-like phase by 51.73 +/- 8.5% without affecting the interictal-like phase of the Cs-FP. DIDS (50 uM), a nonselective antagonist of Cl(-)/HCO3(-)-exchangers, Na(+)-HCO3(-)-cotransporters, chloride channels and KCC2, suppressed the ictal-like phase by 60.8 +/- 8.1% without affecting the interictal-like phase. At 500 uM, DIDS completely suppressed the Cs-FP. Based on these results we propose that the anticonvulsant action of furosemide in the Cs(+)-model is exerted through blockade of the neuronal KCC2 and Na(+)-independent Cl(-)/HCO3(-)-exchanger (AE3) leading to stabilization of the activity-induced intracellular acidification in CA1 pyramidal neurons.

PMID:26301821 Uwera J et al; Brain Res 1625: 1-8 (2015)


Sodium chloride reabsorption in the thick ascending limb of the loop of Henle is mediated by the Na(+)-K(+)-2Cl(-) cotransporter (NKCC2). The loop diuretic furosemide is a potent inhibitor of NKCC2. However, less is known about the mechanism regulating the electrolyte transporter. Considering the well-established effects of nitric oxide on NKCC2 activity, cGMP is likely involved in this regulation. cGMP-dependent protein kinase I (cGKI; PKGI) is a cGMP target protein that phosphorylates different substrates after activation through cGMP. We investigated the potential correlation between the cGMP/cGKI pathway and NKCC2 regulation. We treated wild-type (wt) and cGKIa-rescue mice with furosemide. cGKIa-rescue mice expressed cGKIa only under the control of the smooth muscle-specific transgelin (SM22) promoter in a cGKI deficient background. Furosemide treatment increased the urine excretion of sodium and chloride in cGKIa-rescue mice compared to that in wt mice. We analyzed the phosphorylation of NKCC2 by western blotting and immunostaining using the phosphospecific antibody R5. The administration of furosemide significantly increased the phosphorylated NKCC2 signal in wt but not in cGKIa-rescue mice. NKCC2 activation led to its phosphorylation and membrane translocation. To examine whether cGKI was involved in this process, we analyzed vasodilator-stimulated phosphoprotein, which is phosphorylated by cGKI. Furosemide injection resulted in increased vasodilator-stimulated phosphoprotein phosphorylation in wt mice. We hypothesize that furosemide administration activated cGKI, leading to NKCC2 phosphorylation and membrane translocation. This cGKI-mediated pathway could be a mechanism to compensate for the inhibitory effect of furosemide on NKCC2.

PMID:26183401 Limmer F et al; FEBS J 282 (19): 3786-98 (2015)


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  • TABLET;ORAL - 20MG
  • TABLET;ORAL - 40MG
  • TABLET;ORAL - 80MG
  • INJECTABLE;INJECTION - 10MG/ML **Federal Register determination that product was not discontinued or withdrawn for safety or effectiveness reasons**
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