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budralazine (Buterazine / budralazine)

✓ Approved

Daiichi Sankyo Company Limited · CACNA1C · Small Molecule

What is budralazine?

budralazine is a small molecule developed by Daiichi Sankyo Company Limited. It is approved for therapeutic indications.

Drug Profile

Brand NamesButerazine, budralazine
CompanyDaiichi Sankyo Company Limited
Drug ClassSmall Molecule
Molecular TargetCACNA1C
StatusApproved
Sources: ClinicalTrials.gov, Daiichi Sankyo Company Limited

Mechanism of Action

Molecular Targets

budralazine acts on 1 molecular target:

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

budralazine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedNihon Ronen Igakkai zasshi. Japanese journal of geriatrics1999-08-31

[Multicenter prospective survey of prognosis of hypertensive elderly outpatient under antihypertensive treatment--morbidity and mortality of cardiovascular diseases and cancer].

Ogihara T T, Morimoto S S, Nakahashi T T, Hiwada K K et al.

Although calcium-channel blockers and angiotensin-I-converting enzyme inhibitors are often used for treatment of hypertension in the elderly in Japan compared to those in the United States and in European countries, there have been few investigations on the prognosis of the elderly receiving these antihypertensive treatments. The Research Group for "Guidelines on the Treatment of Hypertension in the Elderly" collaborated with the Comprehensive Research Projects on Aging and Health group of the Ministry of Health and Welfare of Japan in performing a 3-year survey on the outcome of 700 hypertensive elderly outpatients (> or = 60 years) receiving treatment of antihypertensive drugs. Antihypertensive drugs including dihydropyridine-type calcium channel blockers, beta blockers, angiotensin-I-converting enzyme inhibitors, diltiazem, diuretics and old-type antihypertensives (hydralazine, budralazine, and centrally acting drugs such as clonidine, methyldopa and guanabenz) were administered to 71.3%, 30.4%, 26.2%, 14.0%, 8.6%, and 6.4% of the 642 elderly patients surveyed for three years, at the time of registration, respectively. Morbidity and mortality rates of total cerebro-cardiovascular diseases, stroke, and heart diseases, were 27.6 and 7.81/1,000 patient-years, 15.1 and 3.6/1,000 patient-years, 10.4 and 4.2/1,000 patient-years, respectively. These results were similar or even better than those of megatrials of antihypertensive treatments for elderly patients in Europe and United States. After adjustment for potential confounding factors, multiple logistic analysis revealed that a past history of ischemic heart disease, use of the old-type antihypertensive drugs, male gender, and diastolic high blood pressure were independent risk factors for the morbidity of cerebro-cardiovascular diseases taking the group of non-cerebro-cardiovascular disease as the reference group. We also identified 22 cases of newly occurred malignancies including 7 fatal cases. However, none of the antihypertensives was significantly related to the occurrence of malignancies. These results lead support to the tendencies in the use of antihypertensive drugs in Japan.

PMID 10466352
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PubMedClinical and experimental hypertension. Part A, Theory and practice1991-01-01

The anti-tachycardic mechanism of a direct-acting vasodilator, budralazine, in rats.

Yoshioka M M, Minami M M, Saito H H

The present study was undertaken to elucidate the anti-tachycardic effect of a direct-acting vasodilator, budralazine, using an electrophysiological technique. Normotensive male Wistar rats were used. Rats were anesthetized intraperitoneally with urethane and alpha-chloralose. Intravenous administration of budralazine (0.5-5.0 mg/kg) produced a dose-dependent reduction of mean arterial pressure in anesthetized rats. At doses of 0.5 and 1.0 mg/kg, budralazine induced bradycardia accompanied with a decrease in cardiac sympathetic nerve activity (ICNA). Preganglionic adrenal sympathetic nerve activity (ASNA) was also reduced by budralazine (1.0 mg/kg). A 0.5 mg/kg of budralazine neither influenced carotid sinus nerve activity nor augmented aortic depressor nerve activity (ADNA). On the contrary, at dose of 5.0 mg/kg, budralazine produced a tachycardia accompanied with increases in both ICNA and ASNA. The ADNA was decreased by budralazine (5.0 mg/kg) significantly. These findings suggest that the central sympathoinhibitory action of budralazine may be responsible for the anti-tachycardic effect of budralazine and baroreceptor-mediated tachycardia occurred after high dose of budralazine.

PMID 1773498
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PubMedJapanese journal of pharmacology1990-08-01

Effects of antihypertensive drugs on experimental cerebral ischemia in spontaneously hypertensive rats.

Tanaka S S, Ashida S S, Akashi A A

The effects of antihypertensive drugs on ischemic cerebral damage were investigated using the bilateral carotid artery occlusion (BCAO) model in SHR. Oral budralazine and nifedipine, at doses that increased cerebral blood flow (CBF) in SHR in our previous study (Tanaka, S. et al., Folia Pharmacol, Japan, 87, 1986), significantly improved cerebral energy failure after the BCAO, but prazosin which does not increase CBF had no effect on the energy failure. These results suggest that the amelioration by these antihypertensive drugs of the energy failure after the BCAO results from its CBF-increasing effects in SHR.

PMID 2214372
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PubMedStroke1989-12-01

Influence of antihypertensive treatment with budralazine on autoregulation of cerebral blood flow in spontaneously hypertensive rats.

Tanaka S S, Tanaka M M, Akashi A A

We studied the effect of chronic antihypertensive treatment with budralazine on the lower blood pressure limit of cerebral blood flow autoregulation using spontaneously hypertensive rats. Cerebral blood flow in the parietal cortex and caudate nucleus was measured to determine the lower limit using the hydrogen clearance method. The lower limit in both cerebral regions was significantly higher in 10 untreated spontaneously hypertensive rats than in 10 Wistar-Kyoto rats. The upward-shifted lower limit was restored to close to normal in the caudate nucleus and was partially restored in the parietal cortex of nine rats by 9 weeks of treatment with the high dose (50-68 mg/kg/day) of budralazine, which kept blood pressure constant at approximately normotension during the treatment period; the lower limit was slightly restored in both cerebral regions of seven rats by 4 weeks of treatment with the high dose. However, 9 weeks of treatment with the low dose (19-27 mg/kg/day) of budralazine, which produced moderate continuous hypotension in nine rats, did not apparently influence the lower limit. Our results suggest that long-term antihypertensive therapy with budralazine reduces the upward-shifted lower blood pressure limit of cerebral blood flow autoregulation toward normal and that the restoration induced by budralazine depends on the degree of blood pressure reduction as well as on the duration of the therapeutic period.

PMID 2595735
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PubMedNihon yakurigaku zasshi. Folia pharmacologica Japonica1989-07-01

[The effect of an antihypertensive drug budralazine on cerebrovascular lesions in salt-loaded SHR].

Tanaka S S, Ishihara M M, Shibamura S S, Sekiguchi F F et al.

Budralazine was evaluated for its protective effect on the onset of cerebrovascular lesions in SHR given 1.5% NaCl as drinking water. The salt-loading for 67 days rapidly accelerated the development of hypertension in SHR (from 180 to over 250 mmHg, 40 days after the loading). The acceleration of hypertension was accompanied by an increase in the incidence of brain softening, cerebral infarct, angionecrosis and hemorrhage by 30-60% following the thrombosis and necrosis of cerebral arterioles. Renal angionecrosis associated with the interstitial nephrosis was also observed by 90% in the animals. Throughout the salt-loading period, oral administration of budralazine (1, 4 and 15 mg/kg/day) resulted in a dose-dependent inhibition of the accelerated hypertension. At larger doses (4 and 15 mg/kg/day), budralazine almost completely ameliorated the cerebral and renal lesions and significantly attenuated the rise of weight in the brain and heart observed in the salt-loaded control rats. Changes in the serum biochemical findings were also inhibited by this drug. In some of the parameters measured, budralazine appeared to be more efficacious than hydralazine (1, 4 and 15 mg/kg/day, p.o.). These results suggest that budralazine attenuates the serious development of hypertension and reduces the incidence and severity of stroke in salt-loaded SHR.

PMID 2792961
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PubMed[Hokkaido igaku zasshi] The Hokkaido journal of medical science1989-05-01

[Anti-tachycardiac effect of a direct-acting vasodilator, budralazine].

Yoshioka M M

The present study was undertaken to elucidate the anti-tachycardiac effect of a direct-acting vasodilator, budralazine, using an electrophysiological technique. Normotensive male Wistar rats were used. Rats were anesthetized intraperitoneally with urethane and alpha-chloralose. After immobilization with gallamine triethiodide, respiration was maintained through a tracheal cannula connected rodent respirator. Intravenous administration of budralazine (0.5, 1.0 and 5.0 mg/kg) produced a dose-dependent reduction of mean arterial pressure. At doses of 0.5 and 1.0 mg/kg, budralazine induced bradycardia accompanied with a decrease in cardiac sympathetic nerve activity. Plasma norepinephrine concentration was reduced by budralazine (0.5 mg/kg). Preganglionic adrenal sympathetic nerve activity was also reduced by budralazine (1.0 mg/kg). A 0.5 mg/kg of budralazine neither influenced carotid sinus nerve activity nor augmented aortic depressor nerve activity. On the contrary, at dose of 5.0 mg/kg, budralazine produced a tachycardia accompanied with increases in both cardiac sympathetic nerve activity. In addition, plasma epinephrine concentration was also increased at a dose of 5.0 mg/kg. The aortic depressor nerve activity was decreased by budralazine (5.0 mg/kg) significantly. When equi-hypotensive doses of budralazine and clonidine were compared, the renal sympathoinhibitory potency of budralazine was less than that of clonidine. These findings suggest that the central sympathoinhibitory action of budralazine may be responsible for the anti-tachycardiac effect of budralazine.

PMID 2767613
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