Drug Information
Drug (ID: DG00829) and It's Reported Resistant Information
Name |
Triamterene
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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)
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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]
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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
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IsoSMILES |
C1=CC=C(C=C1)C2=NC3=C(N=C(N=C3N=C2N)N)N
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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)
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InChIKey |
FNYLWPVRPXGIIP-UHFFFAOYSA-N
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PubChem CID | |||||
ChEBI ID | |||||
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INTEDE ID | |||||
DrugBank ID |
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
Hypertension [ICD-11: BA00]
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Epithelial sodium channel (ENAC) | [1] | |||
Molecule Alteration | Expression | Up-regulation |
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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]
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Epithelial sodium channel (ENAC) | [1] | |||
Molecule Alteration | Expression | Up-regulation |
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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
Edema [ICD-11: MG29]
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Epithelial sodium channel (ENAC) | [1] | |||
Molecule Alteration | Expression | Up-regulation |
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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 |
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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
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