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Auris Medical Achieves Midpoint for Enrollment in Phase 3 Trial of AM-111 in Sudden Deafness

Dual kinase inhibition affords extended in vitro neuroprotection in Aβ toxicity

Gourmaud et al, Journal of Alzheimer’s Disease, 2016, PMID: 27636848
The present study show that PKR (double-stranded RNA dependent kinase) and c-Jun N-terminal kinase (JNK) pathways are actively activated in Aβ-induced neurotoxicity in neuronal cultures and that the dual inhibition of PKR and JNK (using XG-102 and XG-104) nearly completely blocked neuronal death in vitro.

Sub-conjunctival injection of XG-102, a JNK inhibitor peptide, in patients with intraocular inflammation: A safety and tolerability study

Beydoun et al, Journal of Ocular Pharmacology and Therapeutics, 2015, PMID: 25347151
In this clinical trial, XG-102 administered as a single subconjunctival injection as adjunct therapy in patients with recent post-surgery or post-trauma intraocular inflammation is safe and well tolerated.
Complete version (PDF, 188 Kb)

XG-102 administered to healthy male volunteers as a single intravenous infusion: a randomized, double-blind, placebo-controlled, dose-escalating study

Deloche et al, Pharmacology Research & Perspectives, 2014, PMID: 25505576
The present clinical trial concluded that XG-102 single IV doses of 10-80 μg/kg administered over 1 h to healthy male subjects were safe and well tolerated.
Complete version (PDF, 832 Kb)

Efficacy and safety of AM-111 in the treatment of acute sensorineural hearing loss: a double-blind, randomized, placebo-controlled phase II study

Suckfuell et al, Otology Neurology, 2014, PMID: 24979398
The clinical study established proof of concept for AM-111 in the treatment of severe-to-profound acute sensorineural hearing loss (ASNHL). Control for spontaneous hearing recovery is essential for ASNHL studies

Sub-conjunctival injection of XG-102, a c-Jun N-Terminal Kinase inhibitor peptide in the treatment of endotoxin-induced uveitis in rats

El Zaoui et al, Journal of Ocular Pharmacology and Therapeutics, 2014, PMID: 25313830
The study determined optimal XG-102 dose and route of administration in endotoxin-induced uveitis (EIU) in rats with the purpose of clinical study design. The results confirm that XG-102 peptide has potential for treating intraocular inflammation. Sub-conjunctival injection appears as a good compromise to provide a therapeutic effect while limiting side effects.
Complete version (PDF, 499 Kb)

Molecular mechanisms involved in cochlear implantation trauma and the protection of hearing and auditory sensory cells by inhibition of c-Jun-N-terminal kinase signaling

Eshraghi et al, Laryngoscope, 2013, PMID: 23382052
Molecular mechanisms involved in programmed cell death of hair cells [HCs] are different than the ones involved in programmed cell death of supporting cells [SCs]. Local delivery of AM-111 provided a significant level of protection against electrode insertion trauma [EIT]-induced hearing losses, HC losses, and damage to neural elements.

Protection against ischemic cochlear damage by intratympanic administration of AM-111

Omotehara et al, Otology Neurology, 2011, PMID: 22089955
Direct application of AM-111 in gel formulation on the round window was effective in preventing acute hearing loss because of transient cochlear ischemia.  

Auris Medical secures CHF 47.1 mn Series C financing from Sofinnova Ventures and Sofinnova Partners to advance ground-breaking inner ear therapies through Phase III clinical development

A peptide inhibitor of c-Jun N-terminal kinase for the treatment of endotoxin-induced uveitis

Touchard et al, IOVS, 2010, PMID: 20393119
The efficacy of XG-102 in an endotoxin-induced uveitis (EIU) rat model of ocular inflammation using either intravenous or intravitreous administration was determined as well as the biodistribution in ocular tissues.
Complete version (PDF, 4.7 Mb)

D-JNKI-1 treatment prevents the progression of hearing loss in a model of cochlear implantation trauma

Eshraghi et al, Otology Neurology, 2006, PMID: 16791042
Hearing loss caused by cochlear implant electrode insertion trauma in guinea pigs has both acute and delayed components. The delayed component can be prevented by treating the cochlea with D-JNKI-1.

Use of cell-permeable peptides to prevent neuronal degeneration

Borsello et al, Trends in Molecular Medicine, 2004, PMID: 15121051
Neurodegenerative disorders are often associated with loss of neurons condition arising through apoptotic mechanisms. Here, recent findings on the use of cell-permeable peptide inhibiting JNK in in vivo models of neuronal degeneration following ischemia and its potential are reviewed.

A Peptide Inhibitor of c-Jun N-Terminal Kinase Protects against Both Aminoglycoside and Acoustic Trauma-Induced Auditory Hair Cell Death and Hearing Loss

Wang et al, The Journal of Neuroscience, 2003, PMID: 13679429
Hearing loss can be caused by a variety of insults, including acoustic trauma and exposure to ototoxins that principally affect the viability of sensory hair cells via c-Jun N-terminal kinase (JNK) activity. XG-102 was evaluated as a peptide possessing JNK-pathway inhibitory functions to demonstrate its possibilities in otoprotective activities.