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Statistics
Paolasinigaglia.it
Paolasinigaglia.it is hosted in
Italy
.
Paolasinigaglia.it doesn't use HTTPS protocol.
Number of used technologies:
1.
First technologies:
Html,
Number of used javascripts: 0.
Number of used analytics tools:
0.
Its server type is:
Apache.
Technologies in use by Paolasinigaglia.it
Technology
Number of occurences: 1
- Html
Advertisement
Server Type
- Apache
Conversion rate optimization |
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Clickable call number
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Not founded! |
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Conversion form (contact form, subcriber)
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Not founded! |
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Clickable email
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Not founded! |
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CTA (call to action) button
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Not founded! |
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List
|
Not founded! |
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Image
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Not founded! |
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Enhancement
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Not founded! |
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Responsive website
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Not founded! |
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Facebook sharing
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Not founded! |
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Google+ sharing
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Not founded! |
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Twitter sharing
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Not founded! |
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Linkedin sharing
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Not founded! |
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Blog on the webiste
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Not founded! |
HTTPS (SSL) - Paolasinigaglia.it
Missing HTTPS protocol.
Number of occurences: 3
- Name:
Content: text/html; charset=iso-8859-1 - Name: description
Content: Registrazione e gestione dei domini Internet, i documenti necessari, le ultime estensioni possibili, il listino prezzi completo! - Name: keywords
Content: registrazione domini registra rinnova trasferisci il tuo dominio controlla verifica disponibilità dominio tutto compreso
Server / Hosting
- IP: 195.110.124.188
- Latitude: 43.15
- Longitude: 12.11
- Country: Italy
Rname
- ns1.register.it
- ns2.register.it
- mail.register.it
Target
- hostmaster.register.it
HTTP Header Response
HTTP/1.1 200 OK
Date: Tue, 31 May 2016 18:19:46 GMT
Server: Apache
Last-Modified: Fri, 25 Feb 2011 10:24:37 GMT
Accept-Ranges: bytes
Content-Length: 1078
Content-Type: text/html
Content-Language: it
X-Cache: MISS from s_lu10
X-Cache-Lookup: MISS from s_lu10:80
Via: 1.1 s_lu10 (squid/3.5.12)
Connection: keep-alive
DNS
host: paolasinigaglia.it
- class: IN
- ttl: 900
- type: A
- ip: 195.110.124.188
host: paolasinigaglia.it
- class: IN
- ttl: 900
- type: NS
- target: ns1.register.it
host: paolasinigaglia.it
- class: IN
- ttl: 900
- type: NS
- target: ns2.register.it
host: paolasinigaglia.it
- class: IN
- ttl: 900
- type: SOA
- mname: ns1.register.it
- rname: hostmaster.register.it
- serial: 2014041501
- refresh: 10800
- retry: 3600
- expire: 604800
- minimum-ttl: 86400
host: paolasinigaglia.it
- class: IN
- ttl: 900
- type: MX
- pri: 10
- target: mail.register.it
Common Typos/Mistakes
This list shows You some spelling mistakes at internet search for this domain.
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712 North • NOBODY WANTS TO GO BLIND. • Novel small molecules that effectively inhibit a mitochondrial metalloprotease critical for retinal ganglion cells provide a new method for therapeutic intervention in glaucoma, the leading cause of incurable blindness. • Strategic positioning targeting dominant optic atrophy, an orphan disease related to glaucoma. The Problem: Glaucoma – the leading cause of incurable blindness – is a progressive optic neuropathy that leads to irreversible loss of retinal ganglion cells causing diminished visual function and blindness. To date, there are no available therapies that directly target retinal ganglion cells. Instead, all current treatments focus on lowering intraocular pressure, a major risk factor for glaucoma, and only an estimated 30% of patients respond to those therapies. Thus, due to its high incidence, complex etiology, and lack of available therapies, there is an unmet need for neuroprotective drugs to treat glaucoma. The Solution: We are developing neuroprotective drugs to treat glaucoma by targeting the mitochondrial quality control pathway. To this end we are screening for small molecules to identify compounds that can prevent retinal ganglion cell loss. We are initially focusing on dominant optic atrophy, an orphan optic neuropathy with a shared mechanism-of-action, as our fast-to-market solution. In the long term, our therapeutic approach has significant potential to be highly effective in treating other diseases broadly classified as glaucoma. We will bring an innovative solution to a market that hasn’t seen any new approaches to treatment in decades. Market Opportunity: 1 in 30 adults over 40 years have glaucoma, which equates to 64 million people worldwide with 8.4 million being bilaterally blind. In 2013 there were 3.3 million glaucoma patients in the United States, 6.8 million patients in Europe, and 39 million affected individuals in Asia. With an aging population, these numbers are expected to increase to 76 million people worldwide by 2020 and 112 million people by 2040. Dominant optic atrophy is a juvenile optic neuropathy with a minimum prevalence of 1 in 25,000 people with about 12,000 affected people in the United States and 30,000 individuals in Europe. Estimates predict that >50% of patients carry mutations in the Optic Atrophy 1 (OPA1) gene and nearly 20% developed a more severe neuromuscular phenotype. The glaucoma market currently reaches $2.4 billion in the major markets United States, Europe and Japan and is expected to hit $3.0 billion by 2023. Novel classes of intraocular pressure lowering drugs will mainly drive the growth of the glaucoma market, while there are no treatment options available for patients with dominant optic atrophy. The annual treatment costs for a conventional intraocular pressure lowering therapy can range between $150 and $1,200. Neuroprotective therapies can complement intraocular pressure lowering therapies and we estimate the serviceable obtainable market at $600M to $800M. Our strategic positioning to target an orphan optic neuropathy will speed up market entry and allow us to build our reputation as an innovator in ophthalmology and prepare for commercialization for the larger glaucoma market. We estimate the serviceable obtainable market for dominant optic atrophy at $240M to $280M. Competitive Landscape: Several different neuroprotective glaucoma therapies are currently in development, validating this approach to tackling glaucoma. Calcium antagonists have finished phase II trials (Santen) and showed 10% retinal ganglion cell rescue in preclinical studies. Safety trials investigating CNTF as a neuroprotectant for glaucoma have been completed (Neurotech). CNTF showed some protective effects with 15% greater retinal ganglion cell survival after axotomy in preclinical studies. Genetic knockdown of DLK showed 75% retinal ganglion cell rescue upon optic nerve crush and DLK inhibitors are currently being developed (Genentech; Graybug). Alternative approaches are seeking to replace retinal ganglion cells by adoptive cell therapies. Due to the complexity of the disease, we believe there is room for multiple neuroprotective modalities and our approach will most likely complement existing therapies. There are no treatment options for dominant optic atrophy and the pipeline of drugs in development is limited. Preclinical trials with Idebenone (Santhera) showing efficacy in a small sample of patients remain anecdotal and failed to reproduce in animal studies. Also, a damaging effect for healthy retinal ganglion cells was reported. Other ubiquinone analogues (EPI-743, Edison Pharmaceuticals) are under consideration but no studies have been published so far. Even if these therapies successfully enter the market, significant opportunity remains for a superior, functionally distinct therapeutic with orphan drug status to disrupt and take command of the market. The Model: Our goal is to build a sustainable business advancing therapies for eye diseases. We will generate revenue in two ways: product sales and revenue earned through collaboration arrangements. At this stage we are focused on product development by generating a novel therapy for dominant optic atrophy and establishing a drug-development and preclinical testing platform for neurodegenerative diseases. Growth and de-risking strategies include expanding our pipeline of investigational product candidates for dominant optic atrophy, glaucoma and other neurodegenerative diseases and contract research with strategic partners. The Team: We have built a strong team of clinicians, scientists and entrepreneurs (all UCSF Alumni) to make this venture a success. Marcel V. Alavi, PhD has more than a decade of experience in translational vision research and as CEO oversees business strategy and technical development. Luqing Zhang, PhD expert in assay development, Xiaobo Wan, PhD expert in computational chemistry, and Shibing Tang, PhD expert in chemical synthesis. This team is complemented by mentors and advisors with expertise in drug development, drug delivery, and clinical trial design. Timelines: We anticipate that it will take us approximately 4 years from screening to filing an IND, with the following breakdown: 18 months for a proof of concept and to screen for hits. 2 years to generate leads and perform lead optimization, enabling us to select candidate molecules. 12-18 months to conduct IND-enabling studies, file an IND and get ready for a first-in-human trial. In addition we believe that we will be able to speed up the clinical development of our program as orphan drugs require smaller trial sizes. We will also explore the potential for accelerated approval and/or breakthrough status with the FDA. Clinical Development: Glaucoma presents with increasing visual difficulties usually later in life, while dominant optic atrophy classically presents with early childhood onset. Glaucoma is a complex disease with a variety of contributing factors posing challenges in clinical trial design. OPA1 mutations have a high penetrance rate, but the disease is characterized by marked intra- and interfamilial variability. Clinically relevant endpoints for both diseases are structural measurements of the optic disc topography and retinal nerve fiber layer, and visual field changes as measured by standard automated perimetry. The use of these endpoints in clinical trials is potentially limited by the need for large samples, long-term follow-up, and variability of results. About 20% of OPA1 carriers develop neurologic deficits, ranging from early-onset sensorineural deafness to peripheral neuropathy, ataxia, myopathy, and late-onset chronic progressive external ophthalmoplegia. Potential clinically relevant endpoints for these patients are i) functional measures; ii) electrophysiological parameters; and iii) self-assessment-based measurements or quality-of-life measures. With these additional endpoints one can design more robust proof-of-concept trials. Individuals with syndromic dominant optic atrophy are a clearly defined patient population. These patients are also in the strongest need for treatment options. Financials: We have identified the target and we have conceptualized a high throughput assay for small molecule discovery. Our initial goal is to fundraise in order to develop and scale this assay with the goal of a pilot screen together with the Small Molecule Discovery Center at UCSF. We are currently seeking $600K in seed funding to reach this goal. We are also applying for non-dilutive money from the NIH SBIR program, patient organizations, and various business plan competitions to help reach this goal. With a robust high throughput assay we can perform a pilot screen and validate our testing cascade to generate not only high quality tool compounds and potential drug leads, but the preliminary data necessary to make this project attractive for Series A investors or partners.Scottsdale (United States) - 72.167.191.69
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