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    Chemistry

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    Also known as: 20830-75-5, Lanoxin, 12beta-hydroxydigitoxin, Digacin, Dilanacin, Rougoxin
    Molecular Formula
    C41H64O14
    Molecular Weight
    780.9  g/mol
    InChI Key
    LTMHDMANZUZIPE-PUGKRICDSA-N
    FDA UNII
    73K4184T59
    Digoxin
    A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666)
    Digoxin is a Cardiac Glycoside.
    1 2D Structure

    Digoxin

    2 Identification
    2.1 Computed Descriptors
    2.1.1 IUPAC Name
    3-[(3S,5R,8R,9S,10S,12R,13S,14S,17R)-3-[(2R,4S,5S,6R)-5-[(2S,4S,5S,6R)-5-[(2S,4S,5S,6R)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2H-furan-5-one
    2.1.2 InChI
    InChI=1S/C41H64O14/c1-19-36(47)28(42)15-34(50-19)54-38-21(3)52-35(17-30(38)44)55-37-20(2)51-33(16-29(37)43)53-24-8-10-39(4)23(13-24)6-7-26-27(39)14-31(45)40(5)25(9-11-41(26,40)48)22-12-32(46)49-18-22/h12,19-21,23-31,33-38,42-45,47-48H,6-11,13-18H2,1-5H3/t19-,20-,21-,23-,24+,25-,26-,27+,28+,29+,30+,31-,33+,34+,35+,36-,37-,38-,39+,40+,41+/m1/s1
    2.1.3 InChI Key
    LTMHDMANZUZIPE-PUGKRICDSA-N
    2.1.4 Canonical SMILES
    CC1C(C(CC(O1)OC2C(OC(CC2O)OC3C(OC(CC3O)OC4CCC5(C(C4)CCC6C5CC(C7(C6(CCC7C8=CC(=O)OC8)O)C)O)C)C)C)O)O
    2.1.5 Isomeric SMILES
    C[C@@H]1[C@H]([C@H](C[C@@H](O1)O[C@@H]2[C@H](O[C@H](C[C@@H]2O)O[C@@H]3[C@H](O[C@H](C[C@@H]3O)O[C@H]4CC[C@]5([C@@H](C4)CC[C@@H]6[C@@H]5C[C@H]([C@]7([C@@]6(CC[C@@H]7C8=CC(=O)OC8)O)C)O)C)C)C)O)O
    2.2 Other Identifiers
    2.2.1 UNII
    73K4184T59
    2.3 Synonyms
    2.3.1 MeSH Synonyms

    1. Boehringer, Digoxina

    2. Digacin

    3. Digitek

    4. Digoregen

    5. Digoxina Boehringer

    6. Digoxine Nativelle

    7. Dilanacin

    8. Hemigoxine Nativelle

    9. Lanacordin

    10. Lanicor

    11. Lanoxicaps

    12. Lanoxin

    13. Lanoxin Pg

    14. Lanoxin-pg

    15. Lenoxin

    16. Mapluxin

    17. Nativelle, Digoxine

    18. Nativelle, Hemigoxine

    2.3.2 Depositor-Supplied Synonyms

    1. 20830-75-5

    2. Lanoxin

    3. 12beta-hydroxydigitoxin

    4. Digacin

    5. Dilanacin

    6. Rougoxin

    7. Lanoxicaps

    8. Mapluxin

    9. Dynamos

    10. Vanoxin

    11. Davoxin

    12. Digosin

    13. Fargoxin

    14. Natigoxin

    15. Lanocardin

    16. Cordioxil

    17. Digoxinum

    18. Toloxin

    19. Stillacor-

    20. Digoxin Pediatric

    21. Chebi:4551

    22. Mls000069819

    23. Cardiogoxin

    24. Lanacordin

    25. Eudigox

    26. Lanacrist

    27. Lenoxin

    28. Smr000059217

    29. Neo-lanicor

    30. (3beta,5beta,12beta)-3-{[2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl]oxy}-12,14-dihydroxycard-20(22)-enolide

    31. Digoxin Nativelle

    32. Lanoxin Pg

    33. Sk-digoxin

    34. Homolle's Digitalin

    35. Nsc 95100

    36. Nsc-95100

    37. Ncgc00090797-03

    38. 73k4184t59

    39. Dsstox_cid_2934

    40. Digoxin, Analytical Standard

    41. Dsstox_rid_76794

    42. Coragoxine

    43. Dsstox_gsid_22934

    44. Lenoxicaps

    45. Neodioxanin

    46. Cardigox

    47. Cardioxin

    48. Digomal

    49. Lanikor

    50. Lanorale

    51. Purgoxin

    52. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-[(2r,4s,5s,6r)-5-[(2s,4s,5s,6r)-5-[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2h-furan-5-one

    53. Dixina

    54. Grexin

    55. Digon

    56. Dokim

    57. Digitek

    58. Digoxine

    59. Chloroformic Digitalin

    60. Lanoxicaps (tn)

    61. [3h]digoxin

    62. 4-[(1s,2s,5s,7r,10r,11s,14r,15s,16r)-5-{[(2r,4s,5s,6r)-5-{[(2s,4s,5s,6r)-5-{[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy}-4-hydroxy-6-methyloxan-2-yl]oxy}-4-hydroxy-6-methyloxan-2-yl]oxy}-11,16-dihydroxy-2,15-dimethyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadecan-14-yl]-2,5-dihydrofuran-2-one

    63. Smr000653537

    64. Hemigoxine Nativelle

    65. Lanoxin (tn)

    66. [3h]-digoxin

    67. Acygoxin

    68. Digoksyna

    69. Digonix

    70. Digossina

    71. Digoxina

    72. Dimecip

    73. Lifusin

    74. Saroxin

    75. Digos

    76. Digoxin-sandoz

    77. Digoxina-sandoz

    78. Digoxin-zori

    79. Digoxine Navtivelle

    80. Novodigal [inj.]

    81. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-[(2r,4s,5s,6r)-5-[(2s,4s,5s,6r)-5-[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydr

    82. Oxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2h-furan-5-one

    83. Prestwick_170

    84. Digoksyna [polish]

    85. Digossina [dcit]

    86. Cas-20830-75-5

    87. Mfcd00003674

    88. 12a-hydroxydigitoxin

    89. 3b0w

    90. Lanoxin Pediatric

    91. Digoxin [vandf]

    92. Digoxinum [inn-latin]

    93. 12bet.-hydroxydigitoxin

    94. Digoxin [hsdb]

    95. Digoxin [iarc]

    96. Digoxin [inn]

    97. Digoxin [jan]

    98. Digoxigenin-tridigitoxosid

    99. Digoxin [mi]

    100. Digoxina [inn-spanish]

    101. Digoxin [mart.]

    102. Opera_id_1134

    103. Prestwick0_000437

    104. Prestwick1_000437

    105. Prestwick2_000437

    106. Prestwick3_000437

    107. Digoxin (jp17/usp)

    108. Digoxin [usp-rs]

    109. Digoxin [who-dd]

    110. Digoxin [who-ip]

    111. 12 Beta -hydroxydigitoxin

    112. Epitope Id:122964

    113. Chembl1751

    114. Bidd:pxr0148

    115. Schembl20506

    116. Bspbio_000454

    117. Mls001055371

    118. Mls001076495

    119. Digoxin [orange Book]

    120. Digoxin For Peak Identification

    121. Spbio_002393

    122. Digoxin [ep Monograph]

    123. Bpbio1_000500

    124. Gtpl4725

    125. Gtpl4726

    126. Hsdb 214

    127. Digoxin [usp Monograph]

    128. Digoxin [usp:inn:ban:jan]

    129. Digoxin 1.0 Mg/ml In Methanol

    130. Dtxsid5022934

    131. Bdbm46355

    132. Cid_2724385

    133. Digoxinum [who-ip Latin]

    134. Regid_for_cid_2724385

    135. Hms1569g16

    136. Hms2096g16

    137. Hms2232g20

    138. Hms3713g16

    139. Unii-73k4184t59

    140. Digoxigenin-tridigitoxosid [german]

    141. Hy-b1049

    142. Einecs 244-068-1

    143. Tox21_111025

    144. Tox21_201678

    145. Tox21_303050

    146. 20830-75-5 (free)

    147. S4290

    148. Akos015895113

    149. Akos024283494

    150. Zinc242548690

    151. Ccg-220437

    152. Cs-4571

    153. Db00390

    154. Brn 0077011

    155. Ncgc00090797-01

    156. Ncgc00090797-02

    157. Ncgc00090797-04

    158. Ncgc00090797-05

    159. Ncgc00090797-06

    160. Ncgc00090797-07

    161. Ncgc00090797-09

    162. Ncgc00090797-12

    163. Ncgc00090797-15

    164. Ncgc00257022-01

    165. Ncgc00259227-01

    166. As-13281

    167. Card-20(22)-enolide, 3-((o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1-4)-o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1-4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl)oxy)-12,14-dihydroxy-, (3beta,5beta,12beta)-

    168. B7684

    169. D1828

    170. C06956

    171. D00298

    172. 5-18-04-00381 (beilstein Handbook Reference)

    173. 830d755

    174. A814956

    175. Q422222

    176. Sr-01000721866

    177. Digoxin, Certified Reference Material, Tracecert(r)

    178. J-013666

    179. Sr-01000721866-3

    180. Sr-01000721866-4

    181. Brd-k23478508-001-03-7

    182. Digoxin, European Pharmacopoeia (ep) Reference Standard

    183. 0b9662a7-264e-4acd-94b2-9e1138c0ca5a

    184. Digoxin, United States Pharmacopeia (usp) Reference Standard

    185. Digoxin, Pharmaceutical Secondary Standard; Certified Reference Material

    186. 3beta,12beta,14-trihydroxy-5beta,14beta-card-20(22)-enolid-3-tridigitoxosid

    187. Digoxin For Peak Identification, European Pharmacopoeia (ep) Reference Standard

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

    189. (3beta,5beta,12beta)-3-((o-2,6-dideoxy-beta-d-ribo-hexapyranosyl-(1-4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1-4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl)oxy)-12,14-dihydroxycard-20(22)-enolide

    190. 3-[(3s,5r,10s,12r,13s,14s,17r)-3-[(2r,4s,5s,6r)-5-[(2s,4s,5s,6r)-5-[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2h-furan-5-one

    191. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-10,13-dimethyl-3-[(2r,4s,5s,6r)-6-methyl-5-[(2s,4s,5s,6r)-6-methyl-5-[(2s,4s,5s,6r)-6-methyl-4,5-bis(oxidanyl)oxan-2-yl]oxy-4-oxidanyl-oxan-2-yl]oxy-4-oxidanyl-oxan-2-yl]oxy-12,14-bis(oxidanyl)-1,2,3,4,5,6,7,8,9,11,12,

    192. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-[(2r,4s,5s,6r)-5-[(2s,4s,5s,6r)-5-[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyl-tetrahydropyran-2-yl]oxy-4-hydroxy-6-methyl-tetrahydropyran-2-yl]oxy-4-hydroxy-6-methyl-tetrahydropyran-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2h-furan-5-one

    193. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-[(2r,4s,5s,6r)-5-[(2s,4s,5s,6r)-5-[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tet

    194. 3-[(3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-[[(2r,4s,5s,6r)-5-[[(2s,4s,5s,6r)-5-[[(2s,4s,5s,6r)-4,5-dihydroxy-6-methyl-2-oxanyl]oxy]-4-hydroxy-6-methyl-2-oxanyl]oxy]-4-hydroxy-6-methyl-2-oxanyl]oxy]-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,

    195. 3.beta.-((o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1->4)-o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl)oxy)-12.beta.,14-dihydroxy-5.beta.-card-20(22)-enolide

    196. 3beta-((o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1-4)-o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1-4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl)oxy)-12beta,14-dihydroxy-5beta-card-20(22)-enolide

    197. 4-((1s,2s,5s,11s,15s,7r,10r,14r,16r)-5-{5-[5-((2s,4s,5s,6r)-4,5-dihydroxy-6-me Thyl(2h-3,4,5,6-tetrahydropyran-2-yloxy))(4s,5s,2r,6r)-4-hydroxy-6-methyl(2h-3 ,4,5,6-tetrahydropyran-2-yloxy)](4s,5s,2r,6r)-4-hydroxy-6-methyl(2h-3,4,5,6-te Trahydropyran-2-yl

    198. 4-((3s,5r,8r,9s,10s,12r,13s,14s,17r)-3-(((2r,4s,5s,6r)-5-(((2s,4s,5s,6r)-5-(((2s,4s,5s,6r)-4,5-dihydroxy-6-methyltetrahydro-2h-pyran-2-yl)oxy)-4-hydroxy-6-methyltetrahydro-2h-pyran-2-yl)oxy)-4-hydroxy-6-methyltetrahydro-2h-pyran-2-yl)oxy)-12,14-dihydroxy-10,13-dimethylhexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one

    199. 4-[(3s,5r,8r,9s,10s,12r,13s,14s)-3-[(2s,4s,5r,6r)-5-[(2s,4s,5r,6r)-5-[(2s,4s,5r,6r)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyl-oxan-2-yl]oxy-4-hydroxy-6-methyl-oxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-5h-furan-2-one

    200. Card-20(22)-enolide, 3-((o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1->4)-o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl)oxy)-12,14-dihydroxy-,(3.beta.,5.beta.,12.beta.)-

    201. Card-20(22)-enolide, 3-((o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1->4)-o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl)oxy)-12,14-dihydroxy-, (3beta,5beta,12beta)-

    202. Card-20(22)-enolide, 3-((o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1.fwdarw.4)-o-2,6-dideoxy-beta-d-ribo-hexopyranosyl-(1.fwdarw.4)-2,6-dideoxy-beta-d-ribo-hexopyranosyl)oxy)-12,14-dihydroxy-, (3beta,5beta,12beta)-

    203. Card-20(22)-enolide, 3-[[o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1-->4)-o-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl-(1-->4)-2,6-dideoxy-.beta.-d-ribo-hexopyranosyl]oxy]-12,14-dihydroxy-, (3.beta.,5.beta.,12.beta.)-

    2.3.3 Other Synonyms

    1. Lanitop

    2. Methyldigoxin

    3. Medigoxin

    4. Metildigoxin

    2.4 Create Date
    2005-07-19
    3 Chemical and Physical Properties
    Molecular Weight 780.9 g/mol
    Molecular Formula C41H64O14
    XLogP31.3
    Hydrogen Bond Donor Count6
    Hydrogen Bond Acceptor Count14
    Rotatable Bond Count7
    Exact Mass780.42960671 g/mol
    Monoisotopic Mass780.42960671 g/mol
    Topological Polar Surface Area203 Ų
    Heavy Atom Count55
    Formal Charge0
    Complexity1450
    Isotope Atom Count0
    Defined Atom Stereocenter Count21
    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 4  
    Drug NameDigoxin
    PubMed HealthDigoxin
    Drug ClassesAntiarrhythmic, Cardiovascular Agent
    Drug LabelDigoxin Tablets, USP are one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitali...
    Active IngredientDigoxin
    Dosage FormElixir; Injectable; Tablet
    RouteInjection; Oral
    Strength0.05mg/ml; 0.25mg; 0.25mg/ml; 0.125mg
    Market StatusPrescription
    CompanyHikma Maple; Stevens J; Sandoz; Hikma Pharms; Impax Labs; Roxane

    2 of 4  
    Drug NameLanoxin
    PubMed HealthDigoxin
    Drug ClassesAntiarrhythmic, Cardiovascular Agent
    Drug LabelLANOXIN (digoxin) is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium.These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitalis l...
    Active IngredientDigoxin
    Dosage FormTablet; Injectable
    RouteInjection; Oral
    Strength0.0625mg; 0.25mg; 0.25mg/ml; 0.1875mg; 0.125mg
    Market StatusPrescription
    CompanyCovis Injectables; Covis Pharma

    3 of 4  
    Drug NameDigoxin
    PubMed HealthDigoxin
    Drug ClassesAntiarrhythmic, Cardiovascular Agent
    Drug LabelDigoxin Tablets, USP are one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitali...
    Active IngredientDigoxin
    Dosage FormElixir; Injectable; Tablet
    RouteInjection; Oral
    Strength0.05mg/ml; 0.25mg; 0.25mg/ml; 0.125mg
    Market StatusPrescription
    CompanyHikma Maple; Stevens J; Sandoz; Hikma Pharms; Impax Labs; Roxane

    4 of 4  
    Drug NameLanoxin
    PubMed HealthDigoxin
    Drug ClassesAntiarrhythmic, Cardiovascular Agent
    Drug LabelLANOXIN (digoxin) is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium.These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitalis l...
    Active IngredientDigoxin
    Dosage FormTablet; Injectable
    RouteInjection; Oral
    Strength0.0625mg; 0.25mg; 0.25mg/ml; 0.1875mg; 0.125mg
    Market StatusPrescription
    CompanyCovis Injectables; Covis Pharma

    4.2 Therapeutic Uses

    Anti-Arrhythmia Agents; Cardiotonic Agents; Enzyme Inhibitors

    National Library of Medicine's Medical Subject Headings. Digoxin. Online file (MeSH, 2018). Available from, as of August 29, 2018: https://meshb.nlm.nih.gov/search

    /CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Digoxin is included in the database.

    NIH/NLM; ClinicalTrials.Gov. Available from, as of August 29, 2018: https://clinicaltrials.gov/

    Digoxin tablets, USP are indicated for the treatment of mild to moderate heart failure in adults. Digoxin tablets, USP increase left ventricular ejection fraction and improve heart failure symptoms as evidenced by improved exercise capacity and decreased heart failure-related hospitalizations and emergency care, while having no effect on mortality. Where possible, digoxin tablets, USP should be used in combination with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor. /Included in US product label/

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    Digoxin tablets, USP increase myocardial contractility in pediatric patients with heart failure. /Included in US product label/

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    For more Therapeutic Uses (Complete) data for Digoxin (16 total), please visit the HSDB record page.

    4.3 Drug Warning

    Patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation are at high risk of ventricular fibrillation. Treatment of these patients with digoxin leads to greater slowing of conduction in the atrioventricular node than in accessory pathways, and the risks of rapid ventricular response leading to ventricular fibrillation are thereby increased.

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    Cardiac glycosides should be used with caution in patients with severe pulmonary disease, hypoxia, myxedema, acute myocardial infarction, severe heart failure, acute myocarditis (including rheumatic carditis) or an otherwise damaged myocardium, since the likelihood of cardiac glycoside-induced arrhythmias is increased in these patients. The possibility that use of cardiac glycosides in some patients with acute myocardial infarction may result in an undesirable increase in oxygen demand and associated ischemia should be considered. In patients with rheumatic carditis, dosage should be low initially and increased gradually until a beneficial effect is obtained or, if improvement does not occur in these patients, the drug should be discontinued. Cardiac glycosides should be used with caution in patients with chronic constrictive pericarditis since these patients may respond unfavorably. Cardiac glycosides should be administered with extreme caution in patients with acute glomerulonephritis and heart failure; if the drugs are necessary, total daily dosage must be reduced and given in divided doses with constant ECG monitoring. These patients should be treated concomitantly with diuretics and hypotensive agents and the glycoside should be discontinued as soon as possible. Cardiac glycosides also should be used with extreme caution, if at all, in patients with idiopathic hypertrophic subaortic stenosis because increased obstruction to left ventricular outflow may result. Patients with certain disorders involving heart failure associated with preserved left ventricular ejection fraction (e.g., restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, acute cor pulmonale) may be particularly susceptible to the toxicity of cardiac glycosides. /Cardiac glycosides/

    American Society of Health-System Pharmacists; Drug Information 2018. Bethesda, MD. 2018, p. 1814

    Signs and symptoms of digoxin toxicity include anorexia, nausea, vomiting, visual changes and cardiac arrhythmias (first-degree, second-degree (Wenckebach), or third-degree heart block (including asystole); atrial tachycardia with block; AV dissociation; accelerated junctional (nodal) rhythm; unifocal or multiform ventricular premature contractions (especially bigeminy or trigeminy); ventricular tachycardia; and ventricular fibrillation). Toxicity is usually associated with digoxin levels greater than 2 ng/mL although symptoms may also occur at lower levels. Low body weight, advanced age or impaired renal function, hypokalemia, hypercalcemia, or hypomagnesemia may predispose to digoxin toxicity. Obtain serum digoxin levels in patients with signs or symptoms of digoxin therapy and interrupt or adjust dose if necessary. Assess serum electrolytes and renal function periodically.

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    The earliest and most frequent manifestation of digoxin toxicity in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia. The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia. Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmias or alteration in cardiac conduction that develops in a child taking digoxin should initially be assumed to be a consequence of digoxin intoxication.

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    For more Drug Warnings (Complete) data for Digoxin (33 total), please visit the HSDB record page.

    4.4 Minimum/Potential Fatal Human Dose

    Estimated single lethal dose is 10-20 mg.

    Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-153

    4.5 Drug Indication

    Digoxin is indicated in the following conditions: 1) For the treatment of mild to moderate heart failure in adult patients. 2) To increase myocardial contraction in children diagnosed with heart failure. 3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation. In adults with heart failure, when it is clinically possible, digoxin should be administered in conjunction with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor for optimum effects.

    5 Pharmacology and Biochemistry
    5.1 Pharmacology

    Digoxin is a positive inotropic and negative chronotropic drug, meaning that it increases the force of the heartbeat and decreases the heart rate. The decrease in heart rate is particularly useful in cases of atrial fibrillation, a condition characterized by a fast and irregular heartbeat. The relief of heart failure symptoms during digoxin therapy has been demonstrated in clinical studies by increased exercise capacity and reduced hospitalization due to heart failure and reduced heart failure-related emergency medical visits. Digoxin has a narrow therapeutic window. **A note on cardiovascular risk** Digoxin poses a risk of rapid ventricular response that can cause ventricular fibrillation in patients with an accessory atrioventricular (AV) pathway. Cardiac arrest as a result of ventricular fibrillation is fatal. An increased risk of fatal severe or complete heart block is present in individuals with pre-existing sinus node disease and AV block who take digoxin.

    5.2 MeSH Pharmacological Classification

    Anti-Arrhythmia Agents

    Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade. (See all compounds classified as Anti-Arrhythmia Agents.)

    Cardiotonic Agents

    Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)

    Enzyme Inhibitors

    Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)

    5.3 FDA Pharmacological Classification
    5.3.1 Active Moiety
    DIGOXIN
    5.3.2 FDA UNII
    73K4184T59
    5.3.3 Pharmacological Classes
    Cardiac Glycosides [CS]; Cardiac Glycoside [EPC]
    5.4 ATC Code

    C01AA05

    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

    C01 - Cardiac therapy

    C01A - Cardiac glycosides

    C01AA - Digitalis glycosides

    C01AA05 - Digoxin

    5.5 Absorption, Distribution and Excretion

    Absorption

    Digoxin is approximately 70-80% absorbed in the first part of the small bowel. The bioavailability of an oral dose varies from 50-90%, however, oral gelatinized capsules of digoxin are reported to have a bioavailability of 100%. Tmax, or the time to reach the maximum concentration of digoxin was measured to be 1.0 h in one clinical study of healthy patients taking 0.25 mg of digoxin with a placebo. Cmax, or maximum concentration, was 1.32 0.18 ng/ml1 in the same study, and AUC (area under the curve) was 12.5 2.38 ng/ml1. If digoxin is ingested after a meal, absorption is slowed but this does not change the total amount of absorbed drug. If digoxin is taken with meals that are in fiber, absorption may be decreased. **A note on gut bacteria** An oral dose of digoxin may be transformed into pharmacologically inactive products by bacteria in the colon. Studies have indicated that 10% of patients receiving digoxin tablets will experience the degradation of at least 40% of an ingested dose of digoxin by gut bacteria. Several antibiotics may increase the absorption of digoxin in these patients, due to the elimination of gut bacteria, which normally cause digoxin degradation. **A note on malabsorption** Patients with malabsorption due to a variety of causes may have a decreased ability to absorb digoxin. P-glycoprotein, located on cells in the intestine, may interfere with digoxin pharmacokinetics, as it is a substrate of this efflux transporter. P-glycoprotein can be induced by other drugs, therefore reducing the effects of digoxin by increasing its efflux in the intestine.

    Route of Elimination

    The elimination of digoxin is proportional to the total dose, following first order kinetics. After intravenous (IV) administration to healthy subjects, 50-70% of the dose is measured excreted as unchanged digoxin in the urine. Approximately 25 to 28% of digoxin is eliminated outside of the kidney. Biliary excretion appears to be of much less importance than renal excretion. Digoxin is not effectively removed from the body by dialysis, exchange transfusion, or during cardiopulmonary bypass because most of the drug is bound to extravascular tissues.

    Volume of Distribution

    This drug is widely distributed in the body, and is known to cross the blood-brain barrier and the placenta. The apparent volume of distribution of digoxin is 475-500 L. A large portion of digoxin is distributed in the skeletal muscle followed by the heart and kidneys. It is important to note that the elderly population, generally having a decreased muscle mass, may show a lower volume of digoxin distribution.

    Clearance

    The clearance of digoxin closely correlates to creatinine clearance, and does not depend on urinary flow. Individuals with renal impairment or failure may exhibit extensively prolonged half-lives. It is therefore important to titrate the dose accordingly and regularly monitor serum digoxin levels. One pharmacokinetic study measured the mean body clearance of intravenous digoxin to be 88 44ml/min/l.73 m. Another study provided mean clearance values of 53 ml/min/1.73 m in men aged 73-81 and 83 ml/min/1.73 m in men aged 20-33 years old after an intravenous digoxin dose.

    /MILK/ Maximum milk concentrations of 0.96 and 0.61 ng/mL observed at 4-6 hrs after administering single dose of 0.25 mg to 2 women. Maternal plasma concentration slightly higher than concentration in milk.

    Loughnan PM; J Pediatr (St Louis) 92 (6): 1019-20 (1978)

    /MILK/ Digoxin is excreted into breast milk. ... Digoxin milk/plasma ratios have varied from 0.6 to 0.9. Although these amounts seem high, they represent very small amounts of digoxin due to significant maternal protein binding.

    Briggs, G.G., Freeman, R.K., Yaffee, S.J.; Drugs in Pregancy and Lactation Tenth Edition. Wolters Kluwer/Lippincott Williams & Wilkins, Philadelphia, PA. 2015, p. 406

    Following oral administration, peak serum concentrations of digoxin occur at 1 to 3 hours. Absorption of digoxin from digoxin tablets has been demonstrated to be 60 to 80% complete compared to an identical intravenous dose of digoxin (absolute bioavailability). When digoxin tablets are taken after meals, the rate of absorption is slowed, but the total amount of digoxin absorbed is usually unchanged. When taken with meals high in bran fiber, however, the amount absorbed from an oral dose may be reduced.

    NIH; DailyMed. Current Medication Information for Digoxin Tablet (Updated: February 29, 2016). Available from, as of September 4, 2018: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dfac7f13-28be-423d-9389-9089da29da17

    /MILK/ In order to find out whether digoxin therapy of nursing mothers might produce discomfort in suckling infants we have investigated the kinetics of the transfer of digoxin from plasma to milk in 11 nursing mothers. After intravenous or oral application of a single dose of 0.5 mg or 0.75 mg digoxin simultaneous serum, fore- and hindmilk samples were taken. Obviously, a rapid equilibrium occurred between the serum and the milk compartments and there was no difference between fore- and hindmilk. All three digoxin concentration profiles ran parallel with a milk to serum ratio of 0.6 to 0.7. The curves could best be fitted by the sum of two exponential functions. For predicting the digoxin intake into the suckling infant, simulations were carried out on the basis of two coupled compartment models. When the kinetic milk data as well as the kinetic data obtained in infants were fitted by this model it could be shown that even in the case of long half-lives only about 3% of the therapeutic drug levels were reached in the baby. Thus, one can conclude that digoxin accumulation to toxic concentrations should not occur in infants of women treated with appropriate doses of digoxin.

    PMID:7075628 Reinhardt D et al; Eur J Pediatr 138 (1): 49-52 (1982)

    For more Absorption, Distribution and Excretion (Complete) data for Digoxin (19 total), please visit the HSDB record page.

    5.6 Metabolism/Metabolites

    About 13% of a digoxin dose is found to be metabolized in healthy subjects. Several urinary metabolites of digoxin exist, including _dihydrodigoxin_ and _digoxigenin bisdigitoxoside_. Their glucuronidated and sulfated conjugates are thought to be produced through the process of hydrolysis, oxidation, and additionally, conjugation. The cytochrome P-450 system does not play a major role in digoxin metabolism, nor does this drug induce or inhibit the enzymes in this system.

    In most patients, only small amounts of digoxin are metabolized, but the extent of metabolism is variable and may be substantial in some patients. Some metabolism presumably occurs in the liver, but digoxin is also apparently metabolized by bacteria within the lumen of the large intestine following oral administration and possibly after biliary elimination following parenteral administration. The extent of metabolism by bacteria in the large intestine following oral administration appears to vary inversely with the bioavailability of the preparation. Digoxin undergoes stepwise cleavage of the sugar moieties to form digoxigenin-bisdigitoxoside, digoxigenin-monodigitoxoside, and digoxigenin; these metabolites have progressively decreasing cardioactivity. Digoxigenin is subsequently epimerized and/or conjugated to form cardioinactive compounds. Digoxin also undergoes reduction of the lactone ring to form dihydrodigoxin, which also undergoes stepwise cleavage of the sugar moieties to form dihydrodigoxigenin-bisdigitoxoside, dihydrodigoxigenin-monodigitoxoside, and dihydrodigoxigenin; the reduced metabolites are essentially cardioinactive. Some patients may form substantial amounts of the reduced metabolites; data suggest that, in about 10% of patients receiving digoxin, about 40% or more of the drug excreted in urine will consist of reduced metabolites. Because of the rapid and enhanced absorption, use of liquid-filled capsules may minimize the formation of reduced metabolites in such patients. In patients who form substantial amounts of reduced metabolites, alteration of enteric bacterial flora by some anti-infective agents (e.g., erythromycin) may result in a substantial change in digitalization.

    American Society of Health-System Pharmacists; Drug Information 2018. Bethesda, MD. 2018, p. 1821

    5.7 Biological Half-Life

    Digoxin has a half-life of 1.5-2 days in healthy subjects. The half-life in patients who do not pass urine, usually due to renal failure, is prolonged to 3.5-5 days. Since most of the drug is distributed extravascularly, dialysis and exchange transfusion are not optimal methods for the removal of digoxin.

    Eleven mothers given digoxin throughout pregnancy because of rheumatic heart disease were studied. Digoxin was identified in the placenta and, for the first time, in milk. ... The half-life of digoxin in the newborn was 36.2 +/- 5.43 hours (Mean +/- SEM); thus all the digoxin present at birth would be excreted within 10 to 11 days.

    PMID:687540 Chan V et al; Br J Obstet Gynaecol 85 (8): 605-9 (1978)

    Healthy volunteers received 0.4 mg IV/day for 14 days. Half-life 1.54 days. Distribution volume 807 L. Renal clearance 191 mL/min, indicating tubular secretion of digoxin. 1.8 fold accumulation once a day.

    PMID:598412 Keller et al; Eur J Clin Pharmacol 12 (5): 387-92 (1977)

    Values reported for the elimination half life of digoxin in dogs and cats have been highly variable, with vales reported from 14.4-56 hours for dogs; 30-173 hours for cats. Approximate elimination half-lives reported in other special include: sheep 7 hours; horses 17-29 hours; cattle 8 hours.

    Plumb D.C. Veterinary Drug Handbook. 8th ed. (pocket). Ames, IA: Wiley-Blackwell, 2015., p. 440

    The initial (distribution) half-life of digoxin is about 30 minutes after IV administration in both anephric patients and patients with normal renal function. In patients with normal renal function, digoxin has an elimination half-life of 34-44 hours. The elimination half-life of digoxin is prolonged in patients with renal failure; in anephric patients the elimination half-life is about 4.5 days or longer. The elimination half-life is decreased in patients with acute digoxin overdosage. Elimination half-life of digoxin is prolonged in hypothyroid patients and decreased in hyperthyroid patients. In patients with biliary fistulas, plasma half-life is unchanged. In undigitalized patients, institution of fixed daily digoxin maintenance therapy without an initial loading dose results in steady-state plasma concentrations after 4-5 elimination half-life (about 7 days in patients with normal renal function).

    American Society of Health-System Pharmacists; Drug Information 2018. Bethesda, MD. 2018, p. 1821

    Median serum half-life 35 hr in mature newborns and 57 hr in premature newborns.

    PMID:865943 Lang et al; Pediatrics 59 (6): 902-6 (1977)

    5.8 Mechanism of Action

    Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system. It reversibly inhibits the Na-K ATPase enzyme, leading to various beneficial effects. The Na-K ATPase enzyme functions to maintain the intracellular environment by regulating the entry and exit of sodium, potassium, and calcium (indirectly). Na-K ATPase is also known as the _sodium pump_. The inhibition of the sodium pump by digoxin increases intracellular sodium and increases the calcium level in the myocardial cells, causing an increased contractile force of the heart. This improves the left ventricular ejection fraction (EF), an important measure of cardiac function. Digoxin also stimulates the parasympathetic nervous system via the vagus nerve leading to sinoatrial (SA) and atrioventricular (AV) node effects, decreasing the heart rate. Part of the pathophysiology of heart failure includes neurohormonal activation, leading to an increase in norepinephrine. Digoxin helps to decrease norepinephrine levels through activation of the parasympathetic nervous system.

    Cardiac glycosides have been used in the treatment of arrhythmias for more than 200 years. Two-pore-domain (K2P) potassium channels regulate cardiac action potential repolarization. Recently, K2P3.1 [tandem of P domains in a weak inward rectifying K+ channel (TWIK)-related acid-sensitive K+ channel (TASK)-1] has been implicated in atrial fibrillation pathophysiology and was suggested as an atrial-selective antiarrhythmic drug target. We hypothesized that blockade of cardiac K2P channels contributes to the mechanism of action of digitoxin and digoxin. All functional human K2P channels were screened for interactions with cardiac glycosides. Human K2P channel subunits were expressed in Xenopus laevis oocytes, and voltage clamp electrophysiology was used to record K+ currents. Digitoxin significantly inhibited K2P3.1 and K2P16.1 channels. By contrast, digoxin displayed isolated inhibitory effects on K2P3.1. K2P3.1 outward currents were reduced by 80% (digitoxin, 1 Hz) and 78% (digoxin, 1 Hz). Digitoxin inhibited K2P3.1 currents with an IC50 value of 7.4 uM. Outward rectification properties of the channel were not affected. Mutagenesis studies revealed that amino acid residues located at the cytoplasmic site of the K2P3.1 channel pore form parts of a molecular binding site for cardiac glycosides. In conclusion, cardiac glycosides target human K2P channels. The antiarrhythmic significance of repolarizing atrial K2P3.1 current block by digoxin and digitoxin requires validation in translational and clinical studies.

    PMID:29643254 Schmidt C et al; J Pharmacol Exp Ther 365 (3): 614-623 (2018)

    Low concentrations of cardiac glycosides including ouabain, digoxin, and digitoxin block cancer cell growth without affecting Na+,K+-ATPase activity, but the mechanism underlying this anti-cancer effect is not fully understood. Volume-regulated anion channel (VRAC) plays an important role in cell death signaling pathway in addition to its fundamental role in the cell volume maintenance. Here, we report cardiac glycosides-induced signaling pathway mediated by the crosstalk between Na+,K+-ATPase and VRAC in human cancer cells. Submicromolar concentrations of ouabain enhanced VRAC currents concomitantly with a deceleration of cancer cell proliferation. The effects of ouabain were abrogated by a specific inhibitor of VRAC (DCPIB) and knockdown of an essential component of VRAC (LRRC8A), and they were also attenuated by the disruption of membrane microdomains or the inhibition of NADPH oxidase. Digoxin and digitoxin also showed anti-proliferative effects in cancer cells at their therapeutic concentration ranges, and these effects were blocked by DCPIB. In membrane microdomains of cancer cells, LRRC8A was found to be co-immunoprecipitated with Na+,K+-ATPase a1-isoform. These ouabain-induced effects were not observed in non-cancer cells. Therefore, cardiac glycosides were considered to interact with Na+,K+-ATPase to stimulate the production of reactive oxygen species, and they also apparently activated VRAC within membrane microdomains, thus producing anti-proliferative effects.

    PMID:30251696 Fujii T et al; Biochim Biophys Acta Mol Basis Dis 1864 (11): 3792-3804 (2018)

    Cardiac glycosides inhibit the activity of sodium-potassium-activated adenosine triphosphatase (Na+-K+-ATPase), an enzyme required for active transport of sodium across myocardial cell membranes. Inhibition of this enzyme in cardiac cells results in an increase in the contractile state of the heart and it was believed that benefits of cardiac glycosides in heart failure were mainly associated with inotropic action. However, it has been suggested that benefits of cardiac glycosides may be in part related to enzyme inhibition in noncardiac tissues. Inhibition of Na+-K+-ATPase in vagal afferents acts to sensitize cardiac baroreceptors which may in turn decrease sympathetic outflow from the CNS. In addition, by inhibiting Na+-K+-ATPase in the kidney, cardiac glycosides decrease the renal tubular reabsorption of sodium; the resulting increase in the delivery of sodium to the distal tubules leads to the suppression of renin secretion from the kidneys. These observations led to the hypothesis that cardiac glycosides act in heart failure principally by attenuating the activation of the neurohormonal system, rather than by a positive inotropic action. Toxic doses of cardiac glycosides cause efflux of potassium from the myocardium and concurrent influx of sodium. Toxicity results in part from loss of intracellular potassium associated with inhibition of Na+-K+-ATPase. With therapeutic doses, augmentation of calcium influx to the contractile proteins with resultant enhancement of excitation-contraction coupling is involved in the positive inotropic action of cardiac glycosides; the role of Na+-K+-ATPase in this effect is controversial. /Cardiac glycosides/

    American Society of Health-System Pharmacists; Drug Information 2018. Bethesda, MD. 2018, p. 1818

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    API Reference Price

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PADRA DIST."},{"dataSource":"API Import","activeIngredients":"","year":"2023","qtr":"Q3","strtotime":1695493800,"product":"DIGOXIN (NOBILUS) INJECTABLE","address":"ALEMBIC ROAD","city":"GUJARAT","supplier":"C-SQUARED PHARMA","supplierCountry":"POLAND","foreign_port":"FRANKFURT\/MAIN INT\\'L","customer":"ALEMBIC PHARMACEUTICALS LIMITED","customerCountry":"INDIA","quantity":"0.03","actualQuantity":"0.03","unit":"KGS","unitRateFc":"28340","totalValueFC":"1080.3","currency":"USD","unitRateINR":"2989004.7","date":"24-Sep-2023","totalValueINR":"89670.14","totalValueInUsd":"1080.3","indian_port":"Bombay Air","hs_no":"29389010","bill_no":"7989404","productDescription":"API","marketType":"REGULATED MARKET","country":"POLAND","selfForZScoreResived":"Sterile","supplierPort":"FRANKFURT\/MAIN INT\\'L","supplierAddress":"BRIDGE HOUSE UNIT 2,SKEHARD ROAD,T12 H2TK CORK,SDNF IRELAND","customerAddress":"ALEMBIC ROAD"},{"dataSource":"API Import","activeIngredients":"","year":"2024","qtr":"Q3","strtotime":1720636200,"product":"DIGOXIN (NOBILUS) INJECTABLE - (DIGOXIN USP)","address":"ALEMBIC ROAD","city":"GUJARAT","supplier":"C-SQUARED PHARMA","supplierCountry":"POLAND","foreign_port":"FRANKFURT\/MAIN INT\\'L","customer":"ALEMBIC PHARMACEUTICALS LIMITED","customerCountry":"INDIA","quantity":"0.10","actualQuantity":"0.1","unit":"KGS","unitRateFc":"25000","totalValueFC":"5881.9","currency":"USD","unitRateINR":"4916750.6","date":"11-Jul-2024","totalValueINR":"491675.06","totalValueInUsd":"5881.9","indian_port":"Bombay Air","hs_no":"29389010","bill_no":"4455994","productDescription":"API","marketType":"REGULATED MARKET","country":"POLAND","selfForZScoreResived":"Sterile","supplierPort":"FRANKFURT\/MAIN INT\\'L","supplierAddress":"BRIDGE HOUSE UNIT 2SKEHARD ROAD T12 H2TK CORKSDNF IE","customerAddress":"ALEMBIC ROAD"},{"dataSource":"API Import","activeIngredients":"","year":"2024","qtr":"Q4","strtotime":1730053800,"product":"DIGOXIN MICRONIZED (NOBILUS)","address":"PLOT NO.2, MAITRIVIHAR,","city":"HYDERABAD\/ANDHRA PRADESH","supplier":"C-SQUARED PHARMA","supplierCountry":"POLAND","foreign_port":"FRANKFURT\/MAIN INT\\'L","customer":"AUROBINDO PHARMA LIMITED","customerCountry":"INDIA","quantity":"0.10","actualQuantity":"0.1","unit":"KGS","unitRateFc":"18200","totalValueFC":"2351.8","currency":"USD","unitRateINR":"1976149.4","date":"28-Oct-2024","totalValueINR":"197614.94","totalValueInUsd":"2351.8","indian_port":"Hyderabad Air","hs_no":"29389010","bill_no":"6382411","productDescription":"API","marketType":"REGULATED MARKET","country":"POLAND","selfForZScoreResived":"Micronized","supplierPort":"FRANKFURT\/MAIN INT\\'L","supplierAddress":"BRIDGE HOUSE UNIT 2 SKEHARD ROAD, T12 H2TK CORK IRELAND SDNF Ireland","customerAddress":"PLOT NO.2, MAITRIVIHAR,"}]
    13-Jan-2021
    28-Oct-2024
    KGS
    overview
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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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    Aspen API

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    digoxin

    Brand Name : Lanoxin

    Dosage Form : ORAL SOLUTION

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    Digoxin

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    Digoxin

    Brand Name : Lanoxin

    Dosage Form : Digoxin 0.5Mg/2Ml 6 Units Parenteral Use

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    Digoxin

    Brand Name : Lanoxin

    Dosage Form : Injection fluid, resolution

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    Digoxin

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    Digoxin

    Brand Name : Lanoxin

    Dosage Form : LIQ

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    ABRAXIS PHARM

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    DIGOXIN

    Brand Name : DIGOXIN

    Dosage Form : INJECTABLE;INJECTION

    Dosage Strength : 0.25MG/ML

    Approval Date : 1982-01-01

    Application Number : 83217

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    AUROBINDO PHARMA LTD

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    RLD : No

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    DIGOXIN

    Brand Name : DIGOXIN

    Dosage Form : TABLET;ORAL

    Dosage Strength : 0.0625MG

    Approval Date : 2022-02-08

    Application Number : 214982

    RX/OTC/DISCN : RX

    RLD : No

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    AUROBINDO PHARMA LTD

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    RLD : No

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    DIGOXIN

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    Approval Date : 2022-02-08

    Application Number : 214982

    RX/OTC/DISCN : RX

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    RLD : Yes

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    DIGOXIN

    Brand Name : LANOXIN

    Dosage Form : TABLET;ORAL

    Dosage Strength : 0.1875MG

    Approval Date : 1997-09-30

    Application Number : 20405

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    RLD : Yes

    TE Code : AB

    DIGOXIN

    Brand Name : LANOXIN

    Dosage Form : TABLET;ORAL

    Dosage Strength : 0.25MG

    Approval Date : 1997-09-30

    Application Number : 20405

    RX/OTC/DISCN : RX

    RLD : Yes

    TE Code : AB

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    RLD : No

    TE Code :

    DIGOXIN

    Brand Name : LANOXIN

    Dosage Form : TABLET;ORAL

    Dosage Strength : 0.375MG

    Approval Date : 1997-09-30

    Application Number : 20405

    RX/OTC/DISCN : DISCN

    RLD : No

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    RLD : No

    TE Code :

    DIGOXIN

    Brand Name : LANOXIN

    Dosage Form : TABLET;ORAL

    Dosage Strength : 0.5MG

    Approval Date : 1997-09-30

    Application Number : 20405

    RX/OTC/DISCN : DISCN

    RLD : No

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    HIKMA

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    RLD : Yes

    TE Code : AA

    DIGOXIN

    Brand Name : DIGOXIN

    Dosage Form : ELIXIR;ORAL

    Dosage Strength : 0.05MG/ML

    Approval Date : 2004-08-26

    Application Number : 21648

    RX/OTC/DISCN : RX

    RLD : Yes

    TE Code : AA

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    RLD : No

    TE Code : AP

    DIGOXIN

    Brand Name : DIGOXIN

    Dosage Form : INJECTABLE;INJECTION

    Dosage Strength : 0.25MG/ML

    Approval Date : 1982-01-01

    Application Number : 83391

    RX/OTC/DISCN : RX

    RLD : No

    TE Code : AP

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    RLD : No

    TE Code : AA

    DIGOXIN

    Brand Name : DIGOXIN

    Dosage Form : ELIXIR;ORAL

    Dosage Strength : 0.05MG/ML

    Approval Date : 2019-10-04

    Application Number : 213000

    RX/OTC/DISCN : RX

    RLD : No

    TE Code : AA

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    Aspen Pharma Trading Limited,

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    digoxin

    Brand Name : Lanoxin

    Dosage Form : ORAL SOLUTION

    Dosage Strength : 50 MICROGRAM / ML

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    Approval Date :

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    ASPEN PHARMA TRADING LIMITED

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    Dosage Form : Digoxin 0,0625Mg 30 Joined' Oral Use

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    Digoxin

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    Dosage Form : Digoxin 0.5Mg/2Ml 6 Units Parenteral Use

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    Aspen Pharma Trading Limited

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    Digoxin

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    Registration Country : Norway

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    Aspen Pharma Trading Limited

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    Digoxin

    Brand Name : Lanoxin

    Dosage Form : Antic-calc Tablet

    Dosage Strength : 250 mcg

    Packaging : Box

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    Digoxin

    Brand Name : Lanoxin

    Dosage Form : Potion, resolution

    Dosage Strength : 50 mcg/ml

    Packaging : Bottle

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    RIEMSER Pharma GmbH

    Germany
    Pharma Manufacturing 2024
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    Metildigoxin

    Brand Name : Lanitop

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    Ascent Innovative Medicines

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    Ascent Innovative Medicines

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    Ascent Innovative Medicines

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    Ascent Innovative Medicines

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    Ascent Innovative Medicines

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    Ascent Innovative Medicines

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    Belco Pharma

    India
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    Belco Pharma

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    Cooper Pharma Limited

    India
    euroPLX 86 Munich
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    Cooper Pharma Limited

    India
    euroPLX 86 Munich
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    06

    Flagship Biotech International Pvt. Ltd

    India
    euroPLX 86 Munich
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    Regulatory Info : Generic

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    Digoxin

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    Dosage Form : Tablet

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    Regulatory Info : Generic

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    06

    Flagship Biotech International Pvt. Ltd

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    euroPLX 86 Munich
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    India
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    Registration Country : India

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    07

    Holden Medical Laboratories Pvt. Ltd

    India
    euroPLX 86 Munich
    Not Confirmed
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    Holden Medical Laboratories Pvt. Ltd

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    Regulatory Info : Generic

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    Digoxin

    Brand Name :

    Dosage Form : Tablet

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    07

    Holden Medical Laboratories Pvt. Ltd

    India
    euroPLX 86 Munich
    Not Confirmed
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    Holden Medical Laboratories Pvt. Ltd

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    Registration Country : India

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    08

    Holden Medical Laboratories Pvt. Ltd

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    Holden Medical Laboratories Pvt. Ltd

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    Digoxin

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    Dosage Form : Granules

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    Regulatory Info : Generic

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    Holden Medical Laboratories Pvt. Ltd

    India
    euroPLX 86 Munich
    Not Confirmed
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    Holden Medical Laboratories Pvt. Ltd

    India
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    euroPLX 86 Munich
    Not Confirmed
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    Dosage : Granules

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    09

    Infugen Pharma

    India
    euroPLX 86 Munich
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    Infugen Pharma

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    Brand Name :

    Dosage Form : Injection

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    Infugen Pharma

    India
    euroPLX 86 Munich
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    Infugen Pharma

    India
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    Dosage : Injection

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    Registration Country : India

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    10

    Opes Health Care

    India
    euroPLX 86 Munich
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    Opes Health Care

    India
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    euroPLX 86 Munich
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    Digoxin

    Brand Name :

    Dosage Form : Tablet

    Dosage Strength : 250MCG

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    Opes Health Care

    India
    euroPLX 86 Munich
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    Opes Health Care

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    euroPLX 86 Munich
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    Packaging : 3 x 10 Tablets in Blister Pack

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    Dosage : Tablet

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