R&D Pipeline

We designed a new prodrug of rebamipide, called rebamipide mofetil, to overcome the low bioavailability of rebamipide and facilitate systemic absorption via oral administration. SA001 is currently being developed as a world's first oral drug for dry eye syndrome and Sjogren's syndrome. Notably, Sjogren's syndrome is an autoimmune disease that accompanies symptoms of dry eyes and dry mouth, and no drugs have been approved for the fundamental treatment of Sjogren's syndrome to date.

For the patients who are resistant to anti-VEGF therapeutics, a standard therapy for wet age-related macular degeneration (AMD), novel drugs including PDGF antibodies have been under development, but no drugs have been successful in the clinical trials. SJP1803/SJP1804 exerts therapeutic efficacy via a novel mechanism of action which fundamentally inhibits the production of VEGF and VEGF-R in the retina and other lesional tissues. Because SJP1803/1804 acts orthogonal to the current anti-VEGF therapeutics, we expect synergistic therapeutic efficacy when SJP1803/1804 is administered in combination with the current therapies, and SJP1803/1804 can be also a viable treatment option for the patients who have low response rates to the current therapies.

Notably, while the current therapeutics have very poor patient compliance and show severe side effects due to frequent intravitreal injections, SJP1804 is being developed as an eye drop formulation of a novel small molecule which shows greater therapeutic efficacy than the current therapy (Eylea injection), and SJP1803 is being developed as an intravitreal implant that can be administered once every 6 month or a year. Our SJP1803/1804 programs, which have a novel mechanism of action, a non-invasive route of administration, and high patient compliance, will become an innovative therapeutic option that overcomes the limitations of current therapeutics for wet-AMD.

SJP1602 is the world's first dual inhibitor that effectively inhibits the signal transduction induced by FAK1 and Pyk2 (FAK2) which are profoundly overexpressed in cancer and promote tumorigenesis and metastasis. FAK1 and FAK2 are compensatory each other; inhibiting FAK1 signal transduction can activate FAK2 signal transduction which can also drive tumorigenesis and metastasis. Hence, SJP1602, a specific, dual inhibitor of FAK1 and FAK2, can inhibit FAK-induced tumor growth and metastasis more effectively than other FAK inhibitors currently under development. SJP1602 is currently being developed as a novel drug to treat triple-negative breast cancer of which a standard targeted therapy does not exist to date.

In addition, FAK is also known to regulate the development of acquired drug resistance in cancer and the constitution of immunosuppressive tumor microenvironment. Hence, SJP1602 is being developed as a novel combination therapy with chemo- or targeted therapeutic agents to overcome acquired drug resistance in cancer, and as a combination immunotherapy to dramatically boost the response rates of the standard immunotherapeutics by effectively overcoming tumor's immunosuppressive microenvironment.

SJP1604 targets a protein called nucleolin which is profoundly overexpressed on the cell surface of hematologic cancers including acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL), and is being developed to treat standard therapy-resistant hematologic cancers. The significant overexpression of nucleolin has been clearly observed in most of the relapsed/refractory AML patients compared with the healthy people. Thus, we believe that SJP1604 will greatly improve the side-effects and the resistance of the standard therapy and will provide an innovative therapeutic option for refractory hematologic cancer patients including elderly AML, whose 5-year survival rate is only 10%.

The current approaches to develop novel therapeutics for Alzheimer's disease are challenged by great difficulties in fundamentally ceasing the apoptosis of neuron cells which can continue even after the generation and accumulation of beta amyloids and tau proteins are inhibited. Differentiating from the current therapeutic strategies that only target pathogenic proteins such as beta amyloids, we discovered a novel target that is responsible for the regression and the apoptosis of neuron cells by the pathogenic proteins in the brain, and SJP1801 is being developed as a novel drug for Alzheimer's disease, which targets and inhibits the apoptosis of neuron cells as well as the generation of beta-amyloids and tau proteins. Therefore, we believe that SJP1801 will become a groundbreaking therapeutic strategy, which can be also combined with the current therapeutic approaches, in the field of Alzheimer's disease and Parkinson's disease.