Auris Medical Holding AG, Zug, Switzerland—the developer of treatments for acute inner ear tinnitus (AM-101) and acute inner ear hearing loss (AM-111) by way of intratympanic injection— has announced that it is commencing with plans for an initial public offering (IPO) on Nasdaq.
The company says it plans to offer 6.9 million of its common shares (offering) pursuant to a registration statement on Form F-1 with the Securities and Exchange Commission (SEC). In connection with the offering, the company intends to grant the underwriters the option to purchase up to 1,035,000 additional common shares. The estimated price range for the initial public offering is $10.00 to $12.00 per common share. Auris Medical Holding AG has applied to list its common shares on the Nasdaq Global Select Market under the ticker symbol “EARS”. Jefferies LLC and Leerink Partners LLC are acting as joint book-running managers in the proposed IPO. JMP Securities LLC and Needham & Company, LLC are acting as co-managers in the proposed offering.
According to the Auris Medical, the proposed IPO will be made only by means of a prospectus and the registration statement on Form F-1 relating to the proposed offering has been filed with the SEC but has not yet become effective. The common shares to be registered may not be sold nor may offers to buy be accepted prior to the time when the registration statement becomes effective.
AM-101 Post-acute Treatment for Peripheral Tinnitus. In February, The Hearing Review published a news article about the company’s Phase 3 study on its AM-101 treatment for use in the Post-acute Treatment of Peripheral Tinnitus. AM-101 is a small molecule N-methyl-D-aspartate (NMDA) receptor antagonist formulated in a biocompatible gel for intratympanic injection. According to Auris Medical, emerging evidence suggests that NMDA receptors in the cochlea play a major role in the occurrence of tinnitus following inner ear excitotoxicity, which is characterized by excessive synaptic release of glutamate, the principal neurotransmitter in the auditory system. Cochlear excitotoxicity may be triggered by events such as trauma (eg, exposure to excessive noise), neuroinflammation, disturbances in inner ear blood supply (anoxia/ischemia), or the administration of certain ototoxic drugs. It has been proposed that the upregulation of NMDA receptors induced by cochlear excitotoxicity is responsible for aberrant excitation of auditory nerve fibers, which is perceived as tinnitus.
Auris Medical announced in March that results from its phase IIb clinical trial with AM-101 in the treatment of acute inner ear tinnitus were published in Otology & Neurotology. The trial reportedly demonstrated that AM-101 was well tolerated and safe and established proof of concept in the treatment of tinnitus arising from traumatic acoustic injury to the cochlea and otitis media. In particular the trial showed persistent, clinically relevant and statistically significant improvement in several patient-reported tinnitus measures.
The development of AM-101 is based on research conducted at the INSERM Institute for Neurosciences in Montpellier, France. The clinical development of AM-101 was initiated by Auris Medical in 2007 and comprises 3 clinical trials to date. In 2013, Auris Medical reached agreement with the US Food and Drug Administration (FDA) under a Special Protocol Assessment (SPA) for its TACTT2 study, according to the company. Results from its TACTT3 study are expected in late 2015. Patents have been granted in more than 30 countries worldwide so far.
AM-111 for mediation of hair cell death and inflammatory response. In addition to AM-101, Auris Medical is also developing AM-111, a pharmaceutical treatment for acute sensorineural hearing loss. According to Auris Medical, AM-111 received orphan drug designation from both the FDA and EMA for the treatment of ASNHL. The active component of AM-101 is a signal transmitting enzyme that regulates a number of important cellular activities, including activation of genes encoding inflammatory molecules or promoting cell death (apoptosis). JNK is activated following various types of cochlear insults (stress) that may lead to ASNHL. AM-111 enters cells and binds to JNK, thereby inhibiting activation of transcription factors such as c-jun and c-fos. This in turn prevents JNK mediated apoptosis and inflammatory response, which could otherwise result in irreversible loss of hair cells and cochlear neurons. Thus, it is thought that AM-111 will support natural recovery processes and help prevent or reduce chronic hearing loss.
According to Auris Medical, AM-111’s otoprotective effect has been demonstrated in various animal models of cochlear stress, including acute acoustic trauma, acute labyrinthitis (inflammation), drug ototoxicity (aminoglycosides), bacterial infection, cochlear ischemia and cochlear implantation trauma.