Sapresta
Sapresta Uses, Dosage, Side Effects, Food Interaction and all others data.
Sapresta is a novel dihydropyridine derivative that gives rise to two active metabolites (M-1α and M-1β) that exhibit hypotensive activity. It is a calcium antagonist with the formula methyl 2-oxopropyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinedicarboxylate. It was developed by Maruko Seiyaku, introduced by Taiho and launched in Japan in 1997.
Pre-clinical studies with aranidipine and its two metabolites have shown production of increases in femoral blood flow. It has been shown to present potent and long-lasting vasodilating actions. Sapresta and its metabolites are shown to inhibit calcium-induced contraction in isolated rabbit arteries. Studies have shown that aranidipine is more potent to reduce blood pressure than other dihydropyridines. Sapresta produce changes in renal blood flow, this effect may be explained by its effect on alpha-2-adrenoreceptor-mediated vasoconstriction.
| Trade Name | Sapresta |
| Generic | Aranidipine |
| Aranidipine Other Names | Aranidipine |
| Type | |
| Formula | C19H20N2O7 |
| Weight | Average: 388.376 Monoisotopic: 388.127050992 |
| Protein binding | The binding ratio of plasma proteins of aranidipine varies from 84-95%. This ratio of the drug is similar to the unchanged form and for the M-1 metabolite. Most of the binding happens towards serum albumin and a lower amount corresponds to the alpha1-acid glycoprotein. |
| Groups | Experimental |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Sapresta has been used for many years to treat angina pectoris and hypertension.
How Sapresta works
The high potential of aranidipine is thought to be related to the additional calcium antagonistic activity of its metabolite. The mechanism is thought to be related to the capacity of aranidipine and its metabolites to vasodilate afferent and efferent arterioles. this action is performed through the inhibition of voltage-dependent calcium channels. The typical mechanism of action of aranidipine, as all dihydropyridines, is based on the inhibition of L-type calcium channels, decreasing calcium concentration and inducing smooth muscle relaxation. It is a selective alpha2-adrenoreceptor antagonist which inhibits vasoconstrictive responses.
Toxicity
In toxicity studies performed in mice, rats, and beagles there was a reported LD50 of 143 mg/kg, 1982 mg/kg and 4000 mg/kg respectively. In repeated dose studies, some of the reported side effects included increased urinary volume, serum lipid, urea nitrogen, liver weight, decreased urinary osmotic pressure and hypertrophy of hepatocytes. Teratogenic studies showed a slight generation of fetal visceral abnormalities. Other toxicity studies showed no effects on fetal development, reproductive ability, genotoxic, allergenic, or oncogenic potential.
Elimination Route
After administration, aranidipine is rapidly absorbed from the gastrointestinal tract. After absorption, the AUC and Cmax increased linearly in a dose-dependent manner, the Cmax was attained in approximate 3.8-4.8 hours for aranidipine and 4.8-6 hours for the metabolite M-1. The bioavailability of aranidipine in rat, dog, and monkey was about 48%, 41% and 3% respectively.
Half Life
The elimination half-life of aranidipine and the M-1 metabolite are 1.1-1.2 hour and 2.7-3.5 hour respectively.
Elimination Route
Unchanged aranidipine is found in plasma but not in the urine after 1 hour of administration. Just a small amount of drug was found in the bile. These results indicate that the excretion profile of aranidipine is mainly driven by metabolism and not by excretion. When including the metabolites, 52-56% of the original dose is disposed in the urine, 34-45% in feces and 3-4% in expired air. The excretion in the bile was 59% of the administered dose and 63% of this portion is reabsorbed.
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