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1  for moxonidine versus -13.5+/-1.9 mm Hg for guanabenz).
2 e also excited by norepinephrine (50 ng) and guanabenz (10 microg) but not by clonidine (3 microg) or
3 ase at 6 months compared with those on 16 mg guanabenz (4/8; 50%), the historical cohort alone (21/49
4                                              Guanabenz, a metabolism-based irreversible inactivator o
5  Here we demonstrate that treating mice with guanabenz acetate (GA), an FDA-approved antihypertensive
6 gically Active Compounds and discovered that Guanabenz acetate (Wytensin), an FDA-approved drug forme
7 , experimental autoimmune encephalomyelitis, guanabenz alleviates clinical symptoms, which correlates
8                                    Moreover, guanabenz ameliorates relapse in relapsing-remitting exp
9                                              Guanabenz, an alpha2-agonist, prolonged baseline expirat
10                The cytoprotective effects of guanabenz (analogs) have been explained previously by th
11 ingly, robenidine is structurally similar to guanabenz (analogs), which are currently undergoing clin
12 in vivo, we have investigated the effects of guanabenz and N(G)-nitro-L-arginine in HEK 293 cells sta
13  have used two mechanism-based inactivators, guanabenz and NG-amino-L-arginine, to alter the heme/sub
14  The [(o-chlorobenzylidene)amino]guanidines (Guanabenz and Sephin1) have been proposed to exert prote
15 ee specific compounds, namely valproic acid, guanabenz, and a specific Caspase12 inhibitor, achieved
16 at least one adverse event was higher in any guanabenz arm than in the placebo arm, with higher dosin
17 nts did not significantly differ between the guanabenz arms and the placebo.
18     The treatment arms using 64 mg and 32 mg guanabenz, both alone and combined, reached the primary
19  the alpha2-adrenoceptor (alpha2-AR) agonist guanabenz, but not by the Ih-imidazoline receptor agonis
20                            We show here that guanabenz, but not N(G)-nitro-L-arginine, caused the ina
21 demonstrate here that neither robenidine nor guanabenz disrupt the interaction between PPP1R15A and e
22 ver pure alpha(2)-adrenergic agonists (i.e., guanabenz) due to its lowered incidence of sedative side
23 ioral effects of low doses of moxonidine and guanabenz in C57Bl/6 mice in an exploratory arena.
24  stress response using the FDA-approved drug guanabenz increases oligodendrocyte survival in culture
25 ompared to saline-injected controls; whereas guanabenz induced only dose-responsive sedative-like beh
26 -2 adrenergic related side-effect profile of guanabenz is warranted.
27                                        Thus, guanabenz may be a promising therapeutic to minimize inf
28 :1 ratio to receive 64 mg, 32 mg or 16 mg of guanabenz or placebo daily for 6 months as an add-on the
29  complex and constitutive protein synthesis, guanabenz prolonged eIF2alpha phosphorylation in human s
30             Here we show that robenidine and guanabenz protect cells from a tunicamycin-induced unfol
31 by inhibition of Gadd34-PP1 phosphatase with guanabenz protects oligodendrocytes and partially rescue
32 obust preclinical findings demonstrated that guanabenz selectively inhibits endoplasmic reticulum str
33                We describe a small molecule, guanabenz, that bound to a regulatory subunit of protein
34 er signaling cascade, it was possible to use guanabenz to dose-dependently control expression of GLP-
35                                     In vivo, guanabenz treatment protects against oligodendrocyte los
36                                         When guanabenz was administered in the cuprizone model, in wh
37 AR involvement, the sedative-like effects of guanabenz were completely blocked by pretreatment with t
38  how the FDA-approved antihypertensive drug, guanabenz, which has a favorable safety profile and was
39 he clinically licensed antihypertensive drug guanabenz (Wytensin) activates a synthetic signal cascad