Dublin, Ireland
Dublin, Ireland

Opsona Therapeutics is a drug development company specialising in the human immune system and new drugs and vaccines to prevent and treat autoimmune/inflammatory conditions, cancers and infectious diseases.Based in Ireland, Opsona is a spin-out from Trinity College Dublin . Ireland is ranked highly in the world in immunology research, and TCD has been at the forefront of the field.Opsona's research is primarily focused on the role of Toll-like receptors and TLR signalling in human innate immunity. The company was founded in 2004 by three immunologists:Professor Luke O'NeillProfessor Kingston MillsProfessor Dermot KelleherOpsona's main investors are international and life-science focused:Inventages Venture Capital Seroba Bioventures GenenFund Enterprise Ireland ↑ ↑ ↑ ↑ ↑ ↑ ↑ ↑ ↑ ↑ Wikipedia.

SEARCH FILTERS
Time filter
Source Type

Keogh B.,Opsona | Parker A.E.,Opsona
Trends in Pharmacological Sciences | Year: 2011

Since the identification of the first Toll-like receptor (TLR) in humans in 1997, understanding of the molecular basis for innate immunity has increased significantly. The TLR family and downstream signalling pathways have been extensively characterised, There is now significant evidence suggesting a role for TLRs in human inflammatory and immune diseases such as rheumatoid arthritis, diabetes, allergy/asthma and atherosclerosis. Various approaches have been taken to identify novel therapeutic agents targeting TLRs including biologics, small molecules and nucleic acid-based drugs. Several are now being evaluated in the clinic and showing promise against various diseases. This review paper outlines the recent advances in the understanding of TLR biology and highlights novel TLR agonists and antagonists in development for the treatment of immune diseases. © 2011 Elsevier Ltd. All rights reserved.


The present invention provides compounds and methods for the treatment and prophylaxis of renal disease and inflammation. In particular the invention provides methods for the treatment of kidney disease and failure through the administration of compounds which function as inhibitors of TLR2 function and expression.


A composition comprising a TLR2 antagonist for use in the treatment or prophylaxis of pancreatic cancer is provided. In particular, the composition comprises a TLR2 antagonistic antibody which binds specifically to a non-continuous epitope comprising amino acid residues His318, Pro320, Arg321, Tyr323, Lys347, Phe349, Leu371, Glu375, Tyr376 and His398 of human TLR2. Also provided is a pharmaceutical composition comprising the TLR2 antagonist and the chemotherapeutic agent gemcitabine, and further provided is a screening method for the identification of compounds for use in treatment or prevention of pancreatic cancer.


A composition comprising a TLR2 antagonistic antibody or antigen binding fragment thereof for use in the treatment or prophylaxis of pancreatic cancer is provided. The antibody or antigen binding fragment may be provided for simultaneous, separate or sequential administration with a secondary chemotherapeutic agent such as gemcitabine, and optionally a tertiary chemotherapeutic agent such as abraxane for enhanced treatment. Also provided is a screening method for the identification of compounds for use in treatment or prevention of pancreatic cancer.


A composition comprising a TLR2 antagonistic antibody or antigen binding fragment thereof for use in the treatment or prophylaxis of pancreatic cancer is provided. The antibody or antigen binding fragment may be provided for simultaneous, separate or sequential administration with a secondary chemotherapeutic agent such as gemcitabine, and optionally a tertiary chemotherapeutic agent such as abraxane for enhanced treatment. Also provided is a screening method for the identification of compounds for use in treatment or prevention of pancreatic cancer.


A fully humanised antibody having binding specificity to Toll-like Receptor 2 comprises a light chain and a heavy chain entirely comprised of amino acid sequence of human origin. The variable region of the light chain comprises an amino acid sequence which is substantially homologous with the sequence of SEQ ID NO:1, while the variable region of the heavy domain comprises an amino acid sequence which is substantially homologous with the sequence of SEQ ID NO:4. Also provided are nucleic acids encoding such antibodies, as well as the use of the antibodies in medicine, in particular for the treatment of inflammatory and autoimmune diseases which are mediated by Toll-like Receptor 2 activation and signalling.


The present invention relates to the identification of a TLR2 binding epitope wherein binding of a binding member to the epitope serves to inhibit TLR2 activation and/or signalling. Polypeptide fragments of TLR2 and three-dimensional structures comprising one or more amino acid residues His318, Pro320, Gln321 or Arg321, Tyr323, Lys347, Phe349, Leu371, Glu375, Tyr376 and His398 of TLR2 which define the identified epitope are provided for use in generating binding members. Also provided are binding members which bind to the identified epitope and methods of using same for the treatment and/or prevention of conditions associated with TLR2 activation and/or signalling.


A fully humanised antibody having binding specificity to Toll-like Receptor 2 comprising a light chain and a heavy chain entirely comprised of amino acid sequence of human origin. The variable region of the light chain comprises an amino acid sequence which is substantially homologous with the sequence of 5 SEQ ID NO:1, while the variable region of the heavy domain comprises an amino acid sequence which is substantially homologous with the sequence of SEQ ID NO:4. Also provided are nucleic acids encoding such antibodies, as well as the use of the antibodies in medicine, in particular for the treatment of inflammatory and autoimmune diseases which are mediated by Toll-like Receptor 2 activation 10 and signalling.


Grant
Agency: European Commission | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2010.2.4.4-1 | Award Amount: 7.84M | Year: 2010

Delayed graft function (DGF) is defined as the need for dialysis within seven days of renal transplantation (DGF promotes allograft rejection, requires prolonged dialysis and hospitalisation, and increases the likelihood of graft failure and ultimately the duration of renal graft survival-expectancy. The incidence of DGF occurs in 21-44% of cases following cadaveric renal graft. Several rare diseases, particularly those of genetic origin, are associated with the requirement for solid organ transplantation as the disease progresses. At Opsona Therapeutics we have developed a novel antibody (OPN-305) which has received OMP designation (EU/3/09/638) for use in the prevention of DGF. The scientific basis of this development is the inhibition of Toll-like receptor 2 (TLR2)-mediated ischaemic reperfusion injury which has a pivotal role in the pathogenesis of DGF and its sequelae. The MABSOT project is designed to progress the development of this OMP through Phase I and II clinical trial. The successful completion of the programme will allow the continued development of OPN-305 as an OMP for the treatment of DGF in a range of solid organ transplant situations. OPN-305 development will have significant benefit to these patients and health care providers in reducing the prolonged hospitalisation of these individuals, providing greater longevity associated with the transplanted organ and enhanced quality of life for these individuals.


DUBLIN--(BUSINESS WIRE)--Opsona Therapeutics Ltd (‘Opsona’), the innate immune drug development company focused on novel therapeutic approaches to treat oncology, autoimmune and other inflammatory diseases, today announces the preliminary results from its ongoing prospective, open label Phase I/II study being conducted with OPN-305 in second-line lower (Low and intermediate-1) risk myelodysplastic syndrome (MDS) which created interest when presented recently at the 58th Annual Meeting of the American Society of Hematology (ASH) in San Diego by Prof Garcia-Manero from the MD Anderson Cancer Center. OPN-305 is a novel proprietary humanized IgG4 monoclonal antibody (MAb) against Toll-Like Receptor 2 (TLR2), a key target within the innate immune system. Opsona has recently received orphan drug designation from the United States Food and Drug Administration for MDS. The study in patients with lower risk, red cell transfusion dependent, MDS who have failed hypomethylating agents (HMA) ± an erythropoiesis stimulating agent is ongoing in collaboration with MD Anderson Cancer Center in Houston USA with additional sites now being added in the USA. As of December 2016, 24 eligible patients have been enrolled, 11 at 5 mg dose and 13 at 10 mg/kg. A total of 15 (75%) patients are evaluable for response. Hematological improvement has been seen in 53% (8/15) with 3 (20%) patients achieving transfusion independence and of these 2/5 (40%) were receiving 10 mg/kg while on OPN-305 monotherapy. 12 patients remain on study. Median age was 72 years (range 42-87). Nine (43 %) patients were classified as Low risk and 15 (63%) as Intermediate-1 risk by IPSS. Thirteen patients (61%) had diploid cytogenetics, 8 (38%) RAEB,5 (23%) RCMD, 3 (14%) RA, 2 (10%) RARS, and 1 (4%) 5q-, RCMD-RS, CMML. The median number of prior HMA therapies was 2 (range 1-4) with a median duration of prior therapies from time of diagnosis to enrollment of 22.7 months (range 6.3-56.1). The median number of OPN-305 cycles administered is 5 (2-22) with 5 of 9 (55.5%) patients having received azacitidine add-back after 16 weeks of OPN-305 monotherapy. A total of 5 (29%) patients developed AEs related to OPN-305 all grade 1 with gastrointestinal disorders being the most frequent (23.5%). At this point, no significant drug related toxicity or unexpected infectious complications have been seen and combination with azacitidine has been well tolerated. To date three (20%) patients were taken off study due to progression to AML and 4 (27%) due to no response all at the 5 mg/kg dose. There is no evidence of treatment related anti-drug antibodies or statistically significant dynamic changes in cytokines in any of the patients. Myelodysplastic syndromes are a complex and heterogeneous group of bone marrow failure disorders characterized by ineffective hematopoiesis and poor prognosis. There is an urgent need for the development of well tolerated, novel therapies in the treatment of MDS which can delay progression, improve patient survival and quality of life and reduce the social and economic burden of transfusion dependence. Commenting on today’s announcement Mary Reilly VP Pharmaceutical Development & Operations said “OPN-305 data emerging in this heavily pre-treated group of patients is very encouraging, the unmet need for a safe and tolerable product for this patient population is significant and we are happy to be in collaboration with the MD Anderson Cancer Center one of the leading clinical center’s in this hematological area” Opsona is a leading immunology drug development company, focused on novel therapeutic approaches to key targets of the innate immune system associated with a wide range of major human diseases, including cancer, autoimmune and other inflammatory diseases. The company was founded in 2004 by three world-renowned immunologists at Trinity College, Dublin. Opsona has a strong international investor consortium including: Amgen Ventures, BB Biotech Ventures, EMBL Ventures, Enterprise Ireland, Fountain Healthcare Partners, Inventages Venture Capital, Novartis Venture Fund, Omnes Capital, Roche Venture Fund, Seroba Life Sciences, Shire and Sunstone Capital.

Loading Opsona collaborators
Loading Opsona collaborators