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    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
    Furosemide
    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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    01-Jan-2021
    30-Nov-2024
    KGS
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    Average Price (USD/KGS)

    Number of Transactions

    Total Quantity (KGS)

    Total Value (USD)

    Quantity (KGS) & Unit rate (USD/KGS) over time

    API Imports and Exports

    Importing Country Total Quantity
    (KGS)    		 Average Price
    (USD/KGS)    		 Number of Transactions

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    DRUG PRODUCT COMPOSITIONS

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    DOSAGE - TABLET;ORAL - 20MG

    USFDA APPLICATION NUMBER - 16273

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    DOSAGE - TABLET;ORAL - 40MG

    USFDA APPLICATION NUMBER - 16273

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    DOSAGE - TABLET;ORAL - 80MG

    USFDA APPLICATION NUMBER - 16273

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    DOSAGE - INJECTABLE;INJECTION - 10MG/ML **Fed...DOSAGE - INJECTABLE;INJECTION - 10MG/ML **Federal Register determination that product was not discontinued or withdrawn for safety or effectiveness reasons**

    USFDA APPLICATION NUMBER - 18579

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