To evaluate the hypertensive effect of guanbenz acetate, we performed a prospective clinical study for 10 weeks or more in 27 patients with essential hypertension(mean age: 51, mean supine blood pressure: 176/105mmHg). The daily dose of guanabenz acetate was 8-49 mg. The results were as follows; 1) After 2, 4, 6 and 8 weeks of treatment, average supine systolic and diastolic blood pressures reduced to 156/94, 150/94, 149/93 and 144/93mmHg respectively(all P<0.05). 2) Pulse rate decreased slightly from pre-treatment average of 75 beats per minute to 71 beats per minute at the end of the study(P<0.05). 3) Average body weight, serum levels of total cholesterol, AST, ALT, BUN, creatinine, sodium and potassium were not significantly changed from pre-treatment values. 4) A few side effects in order of frequency were dry mouth, dizziness, sedation, weakness, etc. We conclude that guanabenz acetate may be used as an effective first line antihypertensive agent in essential hypertension.
Blood Pressure ; Body Weight ; Cholesterol ; Creatinine ; Dizziness ; Guanabenz* ; Heart Rate ; Humans ; Hypertension ; Mouth ; Potassium ; Prospective Studies ; Sodium

BACKGROUND: Development of chemotherapeutics for the treatment of advanced hepatocellular carcinoma (HCC) has been lagging. Screening of candidate therapeutic agents by using patient-derived preclinical models may facilitate drug discovery for HCC patients. METHODS: Four primary cultured HCC cells from surgically resected tumor tissues and six HCC cell lines were used for high-throughput screening of 252 drugs from the Prestwick Chemical Library. The efficacy and mechanisms of action of the candidate anti-cancer drug were analyzed via cell viability, cell cycle assays, and western blotting. RESULTS: Guanabenz acetate, which has been used as an antihypertensive drug, was screened as a candidate anti-cancer agent for HCC through a drug sensitivity assay by using the primary cultured HCC cells and HCC cell lines. Guanabenz acetate reduced HCC cell viability through apoptosis and autophagy. This occurred via inhibition of growth arrest and DNA damage-inducible protein 34, increased phosphorylation of eukaryotic initiation factor 2α, increased activating transcription factor 4, and cell cycle arrest. CONCLUSIONS: Guanabenz acetate induces endoplasmic reticulum stress–related cell death in HCC and may be repositioned as an anti-cancer therapeutic agent for HCC patients.
Activating Transcription Factor 4 ; Apoptosis ; Autophagy ; Blotting, Western ; Carcinoma, Hepatocellular ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Death ; Cell Line ; Cell Survival ; DNA ; Drug Discovery ; Drug Repositioning ; Endoplasmic Reticulum ; Guanabenz ; Humans ; Mass Screening ; Peptide Initiation Factors ; Phosphorylation ; Primary Cell Culture