The Potential for NX-1207 in Benign Prostatic Hyperplasia: An Update for Clinicians.
The potential for NX-1207 in benign prostatic hyperplasia: an update for clinicians.
Filed under: Drug and Alcohol Rehabilitation
Ther Adv Chronic Dis. 2011 Nov; 2(6): 377-83
Shore N, Cowan B
Lower urinary tract symptoms associated with benign prostatic hyperplasia (BPH) affect many older men and can have a significant impact on health-related quality of life. BPH is a progressive condition that may lead to complications including acute urinary retention. There exists an unmet need for a safe and effective, office-based, catheter-free therapy for BPH patients. NX-1207 is a promising first-in-class drug currently in phase III trials for the treatment of BPH. This review provides an overview of the NX-1207 trial program and considers its potential application for patients with symptoms related to BPH. NX-1207 is administered as an office-based procedure by transrectal intraprostatic injection under ultrasound guidance. NX-1207 has selective pro-apoptotic properties, which induce focal cell loss in prostate tissue, leading to prostate volume reduction with both short- and long-term symptomatic improvement. In four US clinical trials to date, NX-1207 has shown evidence of symptomatic improvement substantially better than currently approved BPH medications with no significant safety issues. Larger phase III trials are ongoing to confirm further the efficacy, safety, and tolerability for this minimally invasive, anesthetic-free, clinic-based treatment for BPH.
HubMed – drug
Retigabine (ezogabine) as add-on therapy for partial-onset seizures: an update for clinicians.
Filed under: Drug and Alcohol Rehabilitation
Ther Adv Chronic Dis. 2011 Nov; 2(6): 371-6
Harris JA, Murphy JA
The present study reviewed the pharmacology, pharmacokinetics, efficacy, and safety of retigabine (ezogabine), a potential agent for use as adjunctive treatment in refractory partial-onset seizures.A MEDLINE search (1966-May 2011) was conducted using the key words retigabine, ezogabine, D-23129, epilepsy, and anticonvulsant. Bibliographies of all articles retrieved were also reviewed. All studies including humans and published in English with data describing retigabine for the adjunctive treatment of partial-onset seizures were reviewed.Retigabine has been shown to interact with the KCNQ2/KCNQ3 subunits of the potassium channels, GABA(A) receptors, and weakly block sodium and calcium channels. Retigabine is 50-60% bioavailable, metabolized by N-glucuronidation and N-acetylation, 80% protein bound, and has few drug-drug interactions. Recent data suggest that retigabine may have a role as adjunctive treatment for refractory partial-onset seizures. Placebo-controlled trials demonstrated a 23.4-44.3% reduction in seizure frequency with 50% responder rates ranging from 23.2% to 47.0% with varying doses of retigabine. The most common adverse effects, occurring in greater than 10% of subjects in the clinical trials, include abnormal gait, confusion, dizziness, fatigue, headache, nausea, somnolence, speech disorder, tremor, urinary tract infection, and blurred vision.Retigabine is a promising agent for adjunctive treatment of refractory partial-onset seizures.
HubMed – drug
Effects of exposure to a DNA damaging agent on the hypoxia inducible factors in organogenesis stage mouse limbs.
Filed under: Drug and Alcohol Rehabilitation
PLoS One. 2012; 7(12): e51937
Huang C, Hales BF
Hypoxia plays a critical role in coordinating cell survival, differentiation and death in normal embryogenesis; during limb pattern formation, hypoxia affects two key processes, chondrogenesis and cell death. Hypoxia promotes chondrocyte differentiation and cartilage matrix synthesis and suppresses terminal differentiation. Depending on the context, hypoxia may induce cell cycle arrest, pro- or anti-apoptotic genes, or autophagy. The response to hypoxia is controlled by hypoxia inducible transcription factors, specifically Hif1a, Hif2a and Hif3a. Under normoxia, the hypoxia-inducible factors respond to a variety of stimuli that include several well established teratogens, such as retinoic acid, heavy metals and hyperglycemia. We hypothesize that teratogenic exposures disrupt limb development by altering the hypoxia signalling pathway. To test this hypothesis, we assessed the effects of a DNA damaging alkylating agent, 4-hydroperoxycyclophosphamide, on the hypoxia inducible factor (HIF) transcription factors and on hypoxia in the murine limb bud culture system. 4-Hydroperoxycyclophosphamide exposure increased HIF1 DNA binding activity and HIF1A and HIF2A, but not HIF3A, protein concentrations. HIF1A and HIF2A immunoreactivities were detected in the apical ectodermal ridge and interdigital regions, where cell death sculpts the limb; 4-hydroperoxycyclophosphamide treatment enhanced their immunoreactivities, specifically in these regions. In contrast, hypoxia was localized to areas of chondrogenesis, the cartilaginous anlagen of the developing long bone and phalanges, and was not enhanced by drug exposure. Thus, the exposure of limb buds in vitro to a DNA damaging teratogen triggered a hypoxia signalling response that was associated with cell death. During limb development the HIFs have oxygen-independent functions.
HubMed – drug
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