Drug (ID: DG00829) and It's Reported Resistant Information
Name
Triamterene
Synonyms
Triamterene; 396-01-0; 6-phenylpteridine-2,4,7-triamine; 2,4,7-Triamino-6-phenylpteridine; Dyrenium; Dytac; Pterofen; Pterophene; Triamteren; Triamteril; Triteren; Ademin; Ademine; Diurene; Noridil; Taturil; Teridin; Urocaudal; Jatropur; Noridyl; Triampur; Diren; Ditak; Dyren; Teriam; Tri-Span; Triamteril complex; Trispan; 6-Phenyl-2,4,7-pteridinetriamine; 2,4,7-Pteridinetriamine, 6-phenyl-; SK&F 8542; 6-Phenyl-2,4,7-triaminopteridine; SKF 8542; Pteridine, 2,4,7-triamino-6-phenyl-; 2,4,7-Triamino-6-fenilpteridina; C12H11N7; UNII-WS821Z52LQ; BRN 0266723; Diucelpin; NSC-77625; SK-8542; WS821Z52LQ; Masuharmin; Triamizide; Triamthiazid; Amteren; Dinazide; Diutensat; Diuteren; Dyberzide; Dytenzide; Esiteren; Hidiurese; Hydrene; Hypertorr; Jenateren; Kalspare; Nephral; Renezide; Reviten; Tricilone; Triurene; Uretren; Diarol; Isobar; Trizid; Anjal; Dazid; Turfa; Apo-triazide; Thiazid Wolff; NCI-C56042; NSC77625; Ademin(e); MFCD00006708; NCGC00016016-10; Triamterena; Triamterenum; CAS-396-01-0; Triazide; Fluss 40; SALI-PUREN; DSSTox_CID_1373; DSSTox_RID_76117; DSSTox_GSID_21373; Triamterenum [INN-Latin]; Triamterena [INN-Spanish]; Dyrenium (TN); CCRIS 5872; Pteridine deriv. 11; HSDB 3405; 2,4,7-Triamino-6-fenilpteridina [Italian]; NCI C56042; SR-01000002968; EINECS 206-904-3; NSC 77625; NSC 639359; AI3-60017; Prestwick_480; SK&F-8542; Dyazide (Salt/Mix); Triamterene [USAN:USP:INN:BAN:JAN]; Spectrum_000508; Triamterene, >=99%; Prestwick0_000034; Prestwick1_000034; Prestwick2_000034; Prestwick3_000034; Spectrum2_000938; Spectrum3_001372; Spectrum4_000366; Spectrum5_001034; Lopac-T-4143; CHEMBL585; T 4143; NCIOpen2_004741; Lopac0_001196; Oprea1_825704; SCHEMBL40707; BSPBio_000127; BSPBio_002924; KBioGR_000831; KBioSS_000988; 5-26-17-00447 (Beilstein Handbook Reference); MLS000069431; BIDD:GT0534; DivK1c_000433; SPECTRUM1500589; SPBio_000876; SPBio_002048; BDBM6644; BPBio1_000141; CHEBI:9671; GTPL4329; Triamterene (JP17/USP/INN); 2,7-Triamino-6-phenylpteridine; 6-Phenyl-2,7-triaminopteridine; DTXSID6021373; HMS501F15; KBio1_000433; KBio2_000988; KBio2_003556; KBio2_006124; KBio3_002144; SKF8542; NINDS_000433; 3'-Bromobiphenyl-3-carboxylicacid; HMS1568G09; HMS2092O17; HMS2095G09; HMS2232B04; HMS3259C08; HMS3263P13; HMS3371D10; HMS3652E10; HMS3712G09; Pharmakon1600-01500589; ZINC120286; 2,7-Pteridinetriamine, 6-phenyl-; Pteridine,4,7-triamino-6-phenyl-; BCP28855; HY-B0575; 2,4,7-triamino-6-phenyl-pteridine; Tox21_110283; Tox21_202021; Tox21_302833; Tox21_501196; CCG-40090; NSC639359; NSC757367; s4080; STK300348; AKOS003790819; Tox21_110283_1; DB00384; LP01196; MCULE-5832721534; NC00544; NSC-639359; NSC-757367; SDCCGSBI-0051163.P004; IDI1_000433; SMP1_000147; NCGC00016016-01; NCGC00016016-02; NCGC00016016-03; NCGC00016016-04; NCGC00016016-05; NCGC00016016-06; NCGC00016016-07; NCGC00016016-08; NCGC00016016-09; NCGC00016016-11; NCGC00016016-12; NCGC00016016-13; NCGC00016016-14; NCGC00016016-15; NCGC00016016-16; NCGC00016016-18; NCGC00016016-28; NCGC00016016-29; NCGC00023458-03; NCGC00023458-04; NCGC00023458-05; NCGC00023458-06; NCGC00023458-07; NCGC00256495-01; NCGC00259570-01; NCGC00261881-01; AC-14066; AS-12471; SMR000059118; SBI-0051163.P003; DB-049442; AB00052116; B2275; BB 0256885; EU-0101196; SW196688-3; T1288; Triamterene 1.0 mg/ml in Dimethyl Sulfoxide; Dyrenium; ; ; 2,4,7-Triamino-6-phenylpteridine; D00386; D95706; WLN: T66 BN DN GN JNJ CZ EZ HR& IZ; AB00052116_13; AB00052116_14; 396T010; A824641; Q221520; SR-01000002968-2; SR-01000002968-4; SR-01000002968-6; BRD-K92049597-001-05-9; BRD-K92049597-001-10-9; Z275128596; Triamterene, British Pharmacopoeia (BP) Reference Standard; Triamterene, European Pharmacopoeia (EP) Reference Standard; Triamterene, United States Pharmacopeia (USP) Reference Standard; Triamterene, Pharmaceutical Secondary Standard; Certified Reference Material
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Indication
In total 3 Indication(s)
Congestive heart failure [ICD-11: BD10-BD1Z]
Approved
[1]
Edema [ICD-11: MG29]
Approved
[1]
Hypertension [ICD-11: BA00]
Approved
[1]
Structure
Drug Resistance Disease(s)
Disease(s) with Clinically Reported Resistance for This Drug (3 diseases)
Edema [ICD-11: MG29]
[1]
Heart failure [ICD-11: BD10]
[1]
Hypertension [ICD-11: BA00]
[1]
Target Amiloride-sensitive sodium channel (ENaC) SCNNA_HUMAN ;
SCNNB_HUMAN ;
SCNNG_HUMAN ;
SCNND_HUMAN
[1]
Click to Show/Hide the Molecular Information and External Link(s) of This Drug
Formula
C12H11N7
IsoSMILES
C1=CC=C(C=C1)C2=NC3=C(N=C(N=C3N=C2N)N)N
InChI
1S/C12H11N7/c13-9-7(6-4-2-1-3-5-6)16-8-10(14)18-12(15)19-11(8)17-9/h1-5H,(H6,13,14,15,17,18,19)
InChIKey
FNYLWPVRPXGIIP-UHFFFAOYSA-N
PubChem CID
5546
ChEBI ID
CHEBI:9671
TTD Drug ID
D00NKB
VARIDT ID
DR01341
INTEDE ID
DR1636
DrugBank ID
DB00384
Type(s) of Resistant Mechanism of This Drug
  ADTT: Aberration of the Drug's Therapeutic Target
Drug Resistance Data Categorized by Their Corresponding Diseases
ICD-11: Circulatory system diseases
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Hypertension [ICD-11: BA00]
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Aberration of the Drug's Therapeutic Target (ADTT) Click to Show/Hide
Key Molecule: Epithelial sodium channel (ENAC) [1]
Molecule Alteration Expression
Up-regulation
Resistant Disease Edema [ICD-11: MG29.0]
Experimental Note Identified from the Human Clinical Data
Mechanism Description In addition to pharmacokinetic effects, compensatory upregulation of sodium transporters not blocked by the diuretic also contributes to diuretic resistance. In patients with CKD, plasma aldosterone levels may be elevated even in the presence of normal plasma renin activity and normal serum potassium concentrations. Elevated plasma levels of both angiotensin II and aldosterone can activate sodium transporters in the distal nephron, including the Na+/Cl cotransporter and ENaC.
Heart failure [ICD-11: BD10]
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Aberration of the Drug's Therapeutic Target (ADTT) Click to Show/Hide
Key Molecule: Epithelial sodium channel (ENAC) [1]
Molecule Alteration Expression
Up-regulation
Resistant Disease Hypertension [ICD-11: BA00.Z]
Experimental Note Identified from the Human Clinical Data
Mechanism Description In addition to pharmacokinetic effects, compensatory upregulation of sodium transporters not blocked by the diuretic also contributes to diuretic resistance. In patients with CKD, plasma aldosterone levels may be elevated even in the presence of normal plasma renin activity and normal serum potassium concentrations. Elevated plasma levels of both angiotensin II and aldosterone can activate sodium transporters in the distal nephron, including the Na+/Cl cotransporter and ENaC.
ICD-21: Symptoms/clinical signs/unclassified clinical findings
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Edema [ICD-11: MG29]
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Aberration of the Drug's Therapeutic Target (ADTT) Click to Show/Hide
Key Molecule: Epithelial sodium channel (ENAC) [1]
Molecule Alteration Expression
Up-regulation
Resistant Disease Congestive heart failure [ICD-11: BD10.1]
Experimental Note Identified from the Human Clinical Data
Mechanism Description In addition to pharmacokinetic effects, compensatory upregulation of sodium transporters not blocked by the diuretic also contributes to diuretic resistance. In patients with CKD, plasma aldosterone levels may be elevated even in the presence of normal plasma renin activity and normal serum potassium concentrations. Elevated plasma levels of both angiotensin II and aldosterone can activate sodium transporters in the distal nephron, including the Na+/Cl cotransporter and ENaC.
Key Molecule: Epithelial sodium channel (ENAC) [1]
Molecule Alteration Expression
Up-regulation
Resistant Disease Human immunodeficiency virus infection [ICD-11: 1C62.0]
Experimental Note Identified from the Human Clinical Data
Mechanism Description In addition to pharmacokinetic effects, compensatory upregulation of sodium transporters not blocked by the diuretic also contributes to diuretic resistance. In patients with CKD, plasma aldosterone levels may be elevated even in the presence of normal plasma renin activity and normal serum potassium concentrations. Elevated plasma levels of both angiotensin II and aldosterone can activate sodium transporters in the distal nephron, including the Na+/Cl cotransporter and ENaC.
References
Ref 1 Diuretic Resistance .Am J Kidney Dis. 2017 Jan;69(1):136-142. doi: 10.1053/j.ajkd.2016.08.027. Epub 2016 Nov 1. 10.1053/j.ajkd.2016.08.027

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