8 results about "Factor D" patented technology

Disclosed herein are monoclonal antibodies that specifically bind to human mature Factor D and that do not bind to human Pro-Factor D, monoclonal antibodies that specifically bind to human Pro-Factor D and do not bind to human mature Factor D, and monoclonal antibodies that bind to both human mature Factor D and human Pro-Factor D. Also disclosed are methods of using the monoclonal antibodies, and compositions comprising the same, for detection of the mature and / or the pro-form of Factor D in biological samples, to determine the status of the Alternative Pathway of Complement (APC) in a mammalian subject, or to determine the status of Factor D after treatment with a MASP-3 inhibitory agent which inhibits the conversion of Pro-Factor D to mature Factor D.

Compounds, methods of use, and processes for making inhibitors of complement Factor D are provided comprising Formula I, I″ and I′″ or a pharmaceutically acceptable salt or composition thereof. The inhibitors described herein target Factor D and inhibit or regulate the complement cascade. The inhibitors of Factor D described herein reduces the excessive activation of complement.

The present invention relates to benzopyrazole compounds and analogs thereof. Disclosed are compounds of Formula (I) and pharmaceutically acceptable salts thereof. The compounds are inhibitors of the complement system. Also provided are pharmaceutical compositions comprising a compound of Formula (I), and methods relating to the use of the compounds and compositions to treat and prevent diseases and conditions characterized by aberrant complement system activity.

Prophylaxis, immune boosting and therapy for vascular complications of diabetes employing various formulations of sulfonic polymers to target and control the activation loop of complement system at C3 level. The molecular targets identified and successfully inhibited are Factor B, Factor D, Factor H. First, this contributes to the inhibition of cross talk pathways in classical and lectin system pathways as well as the C3a and C5a interactions with their receptors. The cross talk pathways inhibit inflammation, oxidative stress, fatty acid synthesis and fibrosis. Secondly, it further inhibits downstream pathways of C5b-9 and also coagulation and thrombotic cascade. Both pathways cause micro vascular and macro vascular complications of diabetes. Thirdly, patient safety is enhanced by Double inhibition of Factor H and Factor D. This reduces adverse effects mediated by individual inhibition of Factor H and Factor D and in addition it has immune boosting effect by targeting immune evasion.

The present application relates to anti-human factor D (FD) antibody constructs. The present application also provides methods of using the anti-human FD antibody constructs to treat complement-mediated diseases, pharmaceutical compositions of the anti-human FD antibody constructs, and methods of making the anti-human FD antibody constructs.

The present invention provides multispecific (e.g., bispecific) constructs that target complement factor D and another complement protein (e.g., C2, C5), nucleic acids encoding such multispecific constructs, and their use for the treatment of complement mediated diseases. Also provided are novel antibody constructs that specifically recognize C5, nucleic acids encoding the antibody constructs, and uses thereof.

The application discloses methods and compositions for the inhibition of the alternative complement pathway. The methods and compositions involve the use of aptamers for inhibiting complement Factor D. The application further provides anti-Factor D aptamers for the treatment of dry age-related macular degeneration, geographic atrophy, wet age-related macular degeneration or Stargardt disease.

Compounds, methods of use, and processes for making inhibitors of complement factor D or a pharmaceutically acceptable salt or composition thereof are provided. The inhibitors described herein target factor D and inhibit or regulate the complement cascade. The inhibitors of factor D described herein reduce the excessive activation of complement.