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188 results on '"Kanes, Stephen J."'

1. Effect of brexanolone on depressive symptoms, anxiety, and insomnia in women with postpartum depression: Pooled analyses from 3 double-blind, randomized, placebo-controlled clinical trials in the HUMMINGBIRD clinical program

Author

Epperson, C. Neill, Rubinow, David R., Meltzer-Brody, Samantha, Deligiannidis, Kristina M., Riesenberg, Robert, Krystal, Andrew D., Bankole, Kemi, Huang, Ming-Yi, Li, Haihong, Brown, Colville, Kanes, Stephen J., and Lasser, Robert

Published
2023
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9. Targeting the Arginine Vasopressin V1b Receptor System and Stress Response in Depression and Other Neuropsychiatric Disorders

Author

Kanes,Stephen J, Dennie,Lara, Perera,Philip, Kanes,Stephen J, Dennie,Lara, and Perera,Philip

Abstract

Stephen J Kanes, Lara Dennie, Philip Perera EmbarkNeuro, Oakland, CA, USACorrespondence: Stephen J Kanes, EmbarkNeuro, Inc, 1111 Broadway, Suite 1300, Oakland, CA, 94607, USA, Tel +1 610 757 7821, Email steve.kanes@embarkneuro.comAbstract: A healthy stress response is critical for good mental and overall health and promotes neuronal growth and adaptation, but the intricately balanced biological mechanisms that facilitate a stress response can also result in predisposition to disease when that equilibrium is disrupted. The hypothalamic-pituitary-adrenal (HPA) axis neuroendocrine system plays a critical role in the body’s response and adaptation to stress, and vasopressinergic regulation of the HPA axis is critical to maintaining system responsiveness during chronic stress. However, exposure to repeated or excessive physical or emotional stress or trauma can shift the body’s stress response equilibrium to a “new normal” underpinned by enduring changes in HPA axis function. Exposure to early life stress due to adverse childhood experiences can also lead to lasting neurobiological changes, including in HPA axis function. HPA axis impairment in patients with depression is considered among the most reliable findings in biological psychiatry, and chronic stress has been shown to play a major role in the pathogenesis and onset of depression and other neuropsychiatric disorders. Modulating HPA axis activity, for example via targeted antagonism of the vasopressin V1b receptor, is a promising approach for patients with depression and other neuropsychiatric disorders associated with HPA axis impairment. Despite favorable preclinical indications in animal models, demonstration of clinical efficacy for the treatment of depressive disorders by targeting HPA axis dysfunction has been challenging, possibly due to the heterogeneity and syndromal nature of depressive disorders. Measures of HPA axis function, such as elevated cortisol levels, may be useful biomarkers for identi

Published
2023

12. Patient-reported health-related quality of life from a randomized, placebo-controlled phase 2 trial of zuranolone in adults with major depressive disorder

Author

Suthoff, Ellison, primary, Kosinski, Mark, additional, Arnaud, Alix, additional, Hodgkins, Paul, additional, Gunduz-Bruce, Handan, additional, Lasser, Robert, additional, Silber, Christopher, additional, Sankoh, Abdul J., additional, Li, Haihong, additional, Werneburg, Brian, additional, Jonas, Jeffrey, additional, Doherty, James, additional, Kanes, Stephen J., additional, and Bonthapally, Vijayveer, additional

Published
2022
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14. Targeting the Arginine Vasopressin V1b Receptor System and Stress Response in Depression and Other Neuropsychiatric Disorders.

Author

Kanes, Stephen J, Dennie, Lara, and Perera, Philip

Subjects
*VASOPRESSIN, *NEUROBEHAVIORAL disorders, *ANXIETY disorders, *HYPOTHALAMIC-pituitary-adrenal axis, *ADVERSE childhood experiences, *NEUROPLASTICITY
Abstract

A healthy stress response is critical for good mental and overall health and promotes neuronal growth and adaptation, but the intricately balanced biological mechanisms that facilitate a stress response can also result in predisposition to disease when that equilibrium is disrupted. The hypothalamic-pituitary-adrenal (HPA) axis neuroendocrine system plays a critical role in the body's response and adaptation to stress, and vasopressinergic regulation of the HPA axis is critical to maintaining system responsiveness during chronic stress. However, exposure to repeated or excessive physical or emotional stress or trauma can shift the body's stress response equilibrium to a "new normal" underpinned by enduring changes in HPA axis function. Exposure to early life stress due to adverse childhood experiences can also lead to lasting neurobiological changes, including in HPA axis function. HPA axis impairment in patients with depression is considered among the most reliable findings in biological psychiatry, and chronic stress has been shown to play a major role in the pathogenesis and onset of depression and other neuropsychiatric disorders. Modulating HPA axis activity, for example via targeted antagonism of the vasopressin V1b receptor, is a promising approach for patients with depression and other neuropsychiatric disorders associated with HPA axis impairment. Despite favorable preclinical indications in animal models, demonstration of clinical efficacy for the treatment of depressive disorders by targeting HPA axis dysfunction has been challenging, possibly due to the heterogeneity and syndromal nature of depressive disorders. Measures of HPA axis function, such as elevated cortisol levels, may be useful biomarkers for identifying patients who may benefit from treatments that modulate HPA axis activity. Utilizing clinical biomarkers to identify subsets of patients with impaired HPA axis function who may benefit is a promising next step in fine-tuning HPA axis activity via targeted antagonism of the V1b receptor. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Effect of Zuranolone vs Placebo in Postpartum Depression

Author

Deligiannidis, Kristina M., primary, Meltzer-Brody, Samantha, additional, Gunduz-Bruce, Handan, additional, Doherty, James, additional, Jonas, Jeffrey, additional, Li, Sigui, additional, Sankoh, Abdul J., additional, Silber, Christopher, additional, Campbell, Andrew D., additional, Werneburg, Brian, additional, Kanes, Stephen J., additional, and Lasser, Robert, additional

Published
2021
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28. A phase 1 double‐blind, placebo‐controlled study of zuranolone (SAGE‐217) in a phase advance model of insomnia in healthy adults.

Author

Bullock, Amy, Gunduz‐Bruce, Handan, Zammit, Gary K., Qin, Min, Li, Haihong, Sankoh, Abdul J., Silber, Christopher, Kanes, Stephen J., Jonas, Jeffrey, and Doherty, James

Subjects
INSOMNIA, ADULTS, BLIND experiment, INSOMNIACS
Abstract

Objective: To evaluate single zuranolone (SAGE‐217) 30 or 45 mg doses in a 5‐h phase advance insomnia model. Methods: In this double‐blind, three‐way crossover study, healthy adults received placebo (n = 41), zuranolone 30 mg (n = 44), and zuranolone 45 mg (n = 42) across three treatment periods. Sleep was assessed by polysomnography and a postsleep questionnaire. Next‐day residual effects and safety/tolerability were evaluated. Results: Compared with placebo, zuranolone resulted in significant improvements in median sleep efficiency (30 mg, 84.6%; 45 mg, 87.6%; placebo, 72.9%; p < 0.001 for both doses), wake after sleep onset (WASO; 30 mg, 55.0 min; 45 mg, 42.5 min; placebo, 113.0 min; p < 0.001 for both doses), duration of awakenings (30 mg, 4.2 min, p < 0.001; 45 mg, 3.7 min, p = 0.001; placebo, 7.4 min), and total sleep time (TST; 30 mg, 406.3 min; 45 mg, 420.3 min; placebo, 350.0 min; p < 0.001 for both doses). Subjective endpoints (WASO, TST, sleep latency, sleep quality) also improved relative to placebo. Zuranolone was generally well tolerated, and the most common adverse events (≥2 participants, any period) were headache and fatigue. Conclusion: Zuranolone improved sleep measures versus placebo in a phase advance model of insomnia in healthy adults, supporting future studies in patients with insomnia disorder. [ABSTRACT FROM AUTHOR]

Published
2022
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35. Trial of SAGE-217 in Patients with Major Depressive Disorder

Author

Gunduz-Bruce, Handan, primary, Silber, Christopher, additional, Kaul, Inder, additional, Rothschild, Anthony J., additional, Riesenberg, Robert, additional, Sankoh, Abdul J., additional, Li, Haihong, additional, Lasser, Robert, additional, Zorumski, Charles F., additional, Rubinow, David R., additional, Paul, Steven M., additional, Jonas, Jeffrey, additional, Doherty, James J., additional, and Kanes, Stephen J., additional

Published
2019
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37. SAGE-217, A Novel GABAA Receptor Positive Allosteric Modulator: Clinical Pharmacology and Tolerability in Randomized Phase I Dose-Finding Studies.

Author

Hoffmann, Ethan, Nomikos, George G., Kaul, Inder, Raines, Shane, Wald, Jeff, Bullock, Amy, Sankoh, Abdul J., Doherty, James, Kanes, Stephen J., and Colquhoun, Helen

Subjects
CLINICAL pharmacology, PHARMACOKINETICS, DRUG tolerance, MENTAL depression, POSTPARTUM depression, STEROID drugs, GABA agonists, SAFETY, BIOCHEMISTRY, RESEARCH, HUMAN research subjects, STEROIDS, HETEROCYCLIC compounds, PHARMACOLOGY, ORAL drug administration, RESEARCH methodology, MEDICAL cooperation, EVALUATION research, DRUG administration, PHENOMENOLOGY, PLACEBOS, COMPARATIVE studies, RANDOMIZED controlled trials, BLIND experiment, DOSE-effect relationship in pharmacology, STATISTICAL sampling, PSYCHOLOGICAL factors
Abstract

Background: SAGE-217, a novel γ-aminobutyric acid A (GABAA) receptor positive allosteric modulator, was evaluated in phase I, double-blind, placebo-controlled, single ascending dose (SAD) and multiple ascending dose (MAD) studies to assess the safety and pharmacokinetics (PK) of SAGE-217 following administration as an oral solution.Methods: In the SAD study, subjects were randomized 6:2 to a single dose of SAGE-217 or placebo. Doses ranged from 0.25 to 66 mg across nine cohorts. In the MAD study, subjects were randomized 9:3 and received SAGE-217 (15, 30, or 35 mg) or placebo once daily for 7 days. In both studies, PK, maximum tolerated dose (MTD; against predetermined criteria), safety, and tolerability were assessed.Results: A total of 108 healthy volunteers enrolled in the studies-72 subjects in the SAD study and 36 subjects in the MAD study. SAGE-217 was orally bioavailable, with a terminal-phase half-life of 16-23 h and a tmax of approximately 1 h. The MTDs for the oral solution of SAGE-217 in the SAD and MAD studies were determined to be 55 and 30 mg daily, respectively. In both studies, SAGE-217 was generally well tolerated, and no serious adverse events (SAEs) were reported. Most AEs were mild, dose-dependent, transient, occurred around the tmax, and related to drug pharmacology.Conclusions: SAGE-217 was generally well tolerated, and its PK profile was well characterized. Based on this profile, SAGE-217 has been advanced into multiple phase II clinical programs and pivotal studies of major depressive disorder and postpartum depression. [ABSTRACT FROM AUTHOR]

Published
2020
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43. Burden of illness for super-refractory status epilepticus patients

Author

Beg, Jamil M., Anderson, Thomas D., Francis, Kevin, Meckley, Lisa M., Fitzhenry, David, Foster, Todd, Sukhtankar, Susheel, Kanes, Stephen J., and Moura, Lidia M. V. R.

Abstract

AbstractObjective:To provide an estimate of the annual number of super-refractory status epilepticus (SRSE) cases in the US and to evaluate utilization of hospital resources by these patients.Methods:The Premier Hospital Database was utilized to estimate the number of SRSE cases based on hospital discharges during 2012. Discharges were classified as SRSE cases based on an algorithm using seizure-related International Classification of Diseases-9 (ICD-9) codes, Intensive Care Unit (ICU) length of stay (LOS), and treatment protocols (e.g. benzodiazepines, anti-epileptic drugs (AEDs), and ventilator use). Secondary analyses were conducted using more restrictive algorithms for SRSE.Results:A total of 6,325 hospital discharges were classified as SRSE cases from a total of 5,300,000 hospital discharges. Applying a weighting based on hospital characteristics and 2012 US demographics, this projected to an estimated 41,156 cases of SRSE in the US during 2012, an estimated incidence rate of ∼13/100,000 annually for SRSE in the US. Secondary analyses using stricter SRSE algorithms resulted in estimated incidence rates of ∼11/100,000 and 8/100,000 annually. The mean LOS for SRSE hospitalizations was 16.5 days (median =11; interquartile range [IQR] = 6–20), and the mean ICU LOS was 9.3 days (median =6; IQR =3–12). The mean cost of an SRSE hospitalization was $51,247 (median = $33,294; 95% CI = $49,634–$52,861).Limitations:The analysis uses ICD-9 diagnostic codes and claims information, and there are inherent limitations in any methodology based on treatment protocol, which created challenges in distinguishing with complete accuracy between SRSE, RSE, and SE on the basis of care patterns in the database.Conclusion:SRSE is associated with high mortality and morbidity, which place a high burden on healthcare resources. Projections based upon the findings of this study suggest an estimated 25,821–41,959 cases of SRSE may occur in the US each year, but more in-depth studies are required.

Published
2017
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45. Olfactory Functioning in Schizophrenia: Relationship to Clinical, Neuropsychological, and Volumetric MRI Measures

Author

Moberg, Paul J., primary, Arnold, Steven E., additional, Doty, Richard L., additional, Gur, Raquel E., additional, Balderston, Catherine C., additional, Roalf, David R., additional, Gur, Ruben C., additional, Kohler, Christian G., additional, Kanes, Stephen J., additional, Siegel, Steven J., additional, and Turetsky, Bruce I., additional

Published
2006
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46. Pharmacokinetic and behavioral characterization of a long-term antipsychotic delivery system in rodents and rabbits

Author

Metzger, Kayla L., primary, Shoemaker, Jody M., additional, Kahn, Jonathan B., additional, Maxwell, Christina R., additional, Liang, Yuling, additional, Tokarczyk, Jan, additional, Kanes, Stephen J., additional, Hans, Meredith, additional, Lowman, Anthony M., additional, Dan, Nily, additional, Winey, Karen I., additional, Swerdlow, Neal R., additional, and Siegel, Steven J., additional

Published
2006
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47. Constitutive Activation of Gαs within Forebrain Neurons Causes Deficits in Sensorimotor Gating Because of PKA-Dependent Decreases in cAMP

Author

Kelly, Michele P, primary, Isiegas, Carolina, additional, Cheung, York-Fong, additional, Tokarczyk, Jan, additional, Yang, Xioaju, additional, Esposito, Michael F, additional, Rapoport, David A, additional, Fabian, Sara A, additional, Siegel, Steven J, additional, Wand, Gary, additional, Houslay, Miles D, additional, Kanes, Stephen J, additional, and Abel, Ted, additional

Published
2006
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49. Corticosterone Modulates Auditory Gating in Mouse

Author

Maxwell, Christina R, primary, Ehrlichman, Richard S, additional, Liang, Yuling, additional, Gettes, David R, additional, Evans, Dwight L, additional, Kanes, Stephen J, additional, Abel, Ted, additional, Karp, Jonathan, additional, and Siegel, Steven J, additional

Published
2005
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