Abstract: The present invention relates to compositions comprising 1-hydroxyl 3,5-bis(4?hydroxyl styryl)benzene or a cosmetically acceptable salt thereof, and methods of treating human skin and signs of skin aging using said compositions.

Abstract: The present invention relates to compositions comprising 1-hydroxyl 3,5-bis(4?hydroxyl styryl)benzene or a cosmetically acceptable salt thereof, and methods of treating human skin and signs of skin aging using said compositions.

Abstract: The present invention relates to compositions comprising 1-hydroxyl 3,5-bis(4?hydroxyl styryl)benzene or a cosmetically acceptable salt thereof, and methods of treating human skin and signs of skin aging using said compositions.

Abstract: The present invention provides CDR-grafted antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CDR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The present invention provides CDR-grated antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CFR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The present invention provides CDR-grated antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CFR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The present invention provides CDR-grated antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CFR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The present invention is directed to the generation of animal models of human disease via the targeted alteration of the nucleic acid sequences in genes encoding drug target proteins. The animal models of human disease may be used for the evaluation of candidate drug molecules.

Abstract: The present invention provides CDR-grated antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CFR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The present invention provides CDR-grafted antibodies against human tissue factor that retain the high binding affinity of rodent monoclonal antibodies against tissue factor but have reduced immunogenicity. The present humanized antibodies are potent anticoagulants and are thus useful in the treatment and prophylaxis of human thrombotic disease. The invention also provides methods of making the CDR-grafted antibodies and pharmaceutical compositions for the attenuation or prevention of coagulation.

Abstract: The binding specificity of the murine OKT3 has been transferred into a human antibody framework in order to reduce its immunogenicity. “Humanized” anti-CD3 mAbs, such as gOKT3-5 and gOKT3-7, have been shown to retain, in vitro, all the properties of native OKT3, including T cell activation which has been correlated, in vivo, with the severe side-effects observed in transplant recipients after the first administration of the mAb. Disclosed are modified versions of humanized anti-CD3 mAbs that do not have the property of T cell activation. Further dislosed are methods of using such mAbs.

Abstract: The binding specificity of the murine OKT3 has been transferred into a human antibody framework in order to reduce its immunogenicity. “Humanized” anti-CD3 mAbs, such as gOKT3-5 and gOKT3-7, have been shown to retain, in vitro, all the properties of native OKT3, including T cell activation which has been correlated, in vivo, with the severe side-effects observed in transplant recipients after the first administration of the mAb. Disclosed are modified versions of humanized anti-CD3 mAbs that do not have the property of T cell activation. Further dislosed are methods of using such mAbs.

Abstract: The present invention provides a whole-cell biological assay that measures changes of endogenous genes under control of an exogenously introduced transcription factor. The exogenous transcription factors of the present invention may be designed such that each is activated by specific extracellular ligands. Therefore cells containing exogenous transcription factors of the present invention provide a generic means to which many extracellular ligands may be tested without undue adaptation to the assay.

Abstract: This invention provides novel neuroprotective 4-pyrimidineamine derivatives and neuroprotective pharmaceutical compositions comprising 4-pyrimidinamines. This invention also provides methods of using these compositions to prevent ischemic cell death, particularly neuronal cell death, and reduce the likelihood of neuronal cell death in a subject due to a traumatic event. Finally, this invention provides an apparatus for administering to a subject the instant pharmaceutical compositions.

Abstract: The binding specificity of the murine OKT3 has been transferred into a human antibody framework in order to reduce its immunogenicity. “Humanized” anti-CD3 mAbs, such as gOKT3-5 and gOKT3-7, have been shown to retain, in vitro, all the properties of native OKT3, including T cell activation which has been correlated, in vivo, with the severe side-effects observed in transplant recipients after the first administration of the mAb. Disclosed are modified versions of humanized anti-CD3 mAbs that do not have the property of T cell activation. Further dislosed are methods of using such mAbs.

Abstract: The binding specificity of the murine OKT3 has been transferred into a human antibody framework in order to reduce its immunogenicity. These “humanized” anti-CD3 monoclonal antibodies retain, in vitro, all the properties of native anti-CD3 antibodies, including T cell activation which has been correlated, in vivo, with the severe side-effects observed in transplant recipients after the first administration of the mAb.

Abstract: The binding specificity of the murine OKT3 has been transferred into a human antibody framework in order to reduce its immunogenicity. This "humanized" anti-CD3 mAb (gOKT3-5) was previously shown to retain, in vitro, all the properties of native OKT3, including T cell activation which has been correlated, in vivo, with the severe side-effects observed in transplant recipients after the first administration of the mAb. Disclosed is a single amino acid mutation from a leucine to a glutamic acid at position 235 in the Fc receptor (FcR) binding segment of the gOKT3-5 mAb to produce Glu-235 mAb. Also disclosed is an amino acid mutation from the contiguous phenylalanine at position 234 to a leucine (Leu-234).

Abstract: The present invention is directed to the dimerization of agonists and antagonists of cell surface receptors and particularly to peptide dimers which behave as cell surface receptor agonists in their dimeric form. Such receptors belong to the dimerization-mediated activation class often observed among receptors for growth and differentiation factors. The agonists of this class of receptors is understood to effect dimerization of the receptor and thus signal initiation. The present invention exemplifies dimers of erythropoietin (EPO) agonists and antagonists comprising a core amino acid sequence of X.sub.3 X.sub.4 X.sub.5 GPX.sub.6 TWX.sub.7 X.sub.8 (SEQ ID NO: 1) wherein each amino acid is indicated by standard one letter abbreviation; X.sub.3 can be C, A, .alpha.-amino-.gamma.-bromobutyric acid or Hoc; X.sub.4 can be R, H, L or W; X.sub.5 can be M, F, or I; X.sub.6 is independently selected from any one of the 20 genetically coded L-amino acids or the stereoisomeric D-amino acids; X.sub.

Abstract: A DNA fragment encoding at least part of the ANF protein has been molecularly cloned and its nucleotide sequence partially determined. The composition and sequence of a peptide containing 116 amino acids within the ANF gene have been determined. Biologically active subunit peptides have been identified.