Molecule Information

General Information of the Molecule (ID: Mol02123)

• Name: Epithelial sodium channel (ENAC) ,Homo sapiens
• Synonyms: ENaC
• Molecule Type: Protein
• Gene Name: ENaC

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  ADTT: Aberration of the Drug's Therapeutic Target

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Triamterene

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Disease Class: Edema [1]

• Resistant Disease: Edema [ICD-11: MG29.0]
• Resistant Drug: Triamterene
• Molecule Alteration: Expression; Up-regulation
• 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.

Disease Class: Congestive heart failure [1]

• Resistant Disease: Congestive heart failure [ICD-11: BD10.1]
• Resistant Drug: Triamterene
• Molecule Alteration: Expression; Up-regulation
• 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.

Disease Class: Human immunodeficiency virus infection [1]

• Resistant Disease: Human immunodeficiency virus infection [ICD-11: 1C62.0]
• Resistant Drug: Triamterene
• Molecule Alteration: Expression; Up-regulation
• 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.

Disease Class: Hypertension [1]

• Resistant Disease: Hypertension [ICD-11: BA00.Z]
• Resistant Drug: Triamterene
• Molecule Alteration: Expression; Up-regulation
• 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