scholarly journals Ansofaxine Hydrochloride

2020 ◽  
Vol 57 (1) ◽  
pp. 87-90
Author(s):  
Vjekoslav Peitl ◽  
Darko Vlahović
Keyword(s):  
Major Depressive Disorder ◽  
Carboxylic Acid ◽  
Environmental Factors ◽  
Depressive Disorder ◽  
Reuptake Inhibitor ◽  
Acid Ester ◽  
Complex Pattern ◽  
Major Depressive ◽  
Ester Prodrug ◽  
Norepinephrine Reuptake

Ansofaxine hydrochloride (LY03005; LPM570065) is a triple reuptake inhibitor that inhibits serotonin, dopamine and norepinephrine reuptake. This novel triple reuptake inhibitor is a carboxylic acid ester prodrug of desvenlafaxine. It is currently under development for the treatment of major depressive disorder - a frequent and heterogeneous disorder induced by a complex pattern of genetic, epigenetic, developmental, and environmental factors.

Remission of major depressive disorder without adverse events: a comparison of escitalopram versus serotonin norepinephrine reuptake inhibitors

2011 ◽  
Vol 27 (6) ◽  
pp. 1089-1096 ◽  
Author(s):  
James Signorovitch ◽  
Karthik Ramakrishnan ◽  
Rym Ben-Hamadi ◽  
Andrew P. Yu ◽  
Eric Q. Wu ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Adverse Events ◽  
Depressive Disorder ◽  
Major Depressive ◽  
Norepinephrine Reuptake

scholarly journals An Underlying Common Factor, Influenced by Genetics and Unique Environment, Explains the Covariation Between Major Depressive Disorder, Generalized Anxiety Disorder, and Burnout: A Swedish Twin Study

2016 ◽  
Vol 19 (6) ◽  
pp. 619-627 ◽  
Author(s):  
Lisa Mather ◽  
Victoria Blom ◽  
Gunnar Bergström ◽  
Pia Svedberg
Keyword(s):  
Risk Factors ◽  
Major Depressive Disorder ◽  
Anxiety Disorder ◽  
Environmental Factors ◽  
Depressive Disorder ◽  
Generalized Anxiety Disorder ◽  
Common Factor ◽  
Generalized Anxiety ◽  
Major Depressive ◽  
Common Pathway

Depression and anxiety are highly comorbid due to shared genetic risk factors, but less is known about whether burnout shares these risk factors. We aimed to examine whether the covariation between major depressive disorder (MDD), generalized anxiety disorder (GAD), and burnout is explained by common genetic and/or environmental factors. This cross-sectional study included 25,378 Swedish twins responding to a survey in 2005–2006. Structural equation models were used to analyze whether the trait variances and covariances were due to additive genetics, non-additive genetics, shared environment, and unique environment. Univariate analyses tested sex limitation models and multivariate analysis tested Cholesky, independent pathway, and common pathway models. The phenotypic correlations were 0.71 (0.69–0.74) between MDD and GAD, 0.58 (0.56–0.60) between MDD and burnout, and 0.53 (0.50–0.56) between GAD and burnout. Heritabilities were 45% for MDD, 49% for GAD, and 38% for burnout; no statistically significant sex differences were found. A common pathway model was chosen as the final model. The common factor was influenced by genetics (58%) and unique environment (42%), and explained 77% of the variation in MDD, 69% in GAD, and 44% in burnout. GAD and burnout had additive genetic factors unique to the phenotypes (11% each), while MDD did not. Unique environment explained 23% of the variability in MDD, 20% in GAD, and 45% in burnout. In conclusion, the covariation was explained by an underlying common factor, largely influenced by genetics. Burnout was to a large degree influenced by unique environmental factors not shared with MDD and GAD.

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