Desmopressin (16679-58-6)

  • For any enquiries about this API or any of Tofigh Daru’s other products, please contact:
  • Contact Us >>

Product Detail

Mechanism:

Upon binding of desmopressin to V2 receptors in the basolateral membrane of the cells of the distal tubule and collecting ducts of the nephron, adenylyl cyclase is stimulated. The resulting intracellular cascades in the collecting duct lead to increased rate of insertion of water channels, called aquaporins, into the lumenal membrane and enhanced the permeability of the membrane to water.
In other words, Desmopressin works by limiting the amount of water that is eliminated in the urine; that is, it is an antidiuretic. It works at the level of the renal collecting duct by binding to V2 receptors, which signal for the translocation of aquaporin channels via cytosolic vesicles to the apical membrane of the collecting duct. The presence of these aquaporin channels in the distal nephron causes increasing water reabsorption from the urine, which becomes passively re-distributed from the nephron to systemic circulation by way of basolateral membrane channels. Desmopressin also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor.

Packaging: polyethylene nylon plastic bag

Storage conditions: In an airtight container, protected from light, at a temperature of 2 °C to 8 °C.

CAS Number:  16679-58-6

Formula: C46H64N14O12S2.xC2H4O2

Molecular Weight: 1069.22

Method of Analysis:  BP Monograph

Application:

Desmopressin (dDAVP), a synthetic analogue of 8-arginine vasopressin (ADH), is an antidiuretic peptide drug modified by deamination of 1-cysteine and substitution of 8-L-arginine by 8-D-arginine. ADH is an endogenous pituitary hormone that has a crucial role in the control of the water content in the body. Upon release from the stimulation of increased plasma osmolarity or decreased circulating blood volume, ADH mainly acts on the cells of the distal part of the nephron and the collecting tubules in the kidney. The hormone interacts with V1, V2 or V3 receptors with differing signal cascade systems.
Desmopressin displays enhanced antidiuretic potency, fewer pressor effects due to V2-selective actions, and a prolonged half-life and duration of action compared to endogenous ADH. It has been employed clinically since 1972, indicated for the treatment of polyuric conditions including primary nocturnal enuresis, nocturia, and diabetes insipidus. It was also newly approved for the treatment of mild classical hemophilia and von Willebrand’s disease for minor surgeries.