Abstract: COVID-19 results from the infection of the SARS-CoV-2 virus and has spread quickly to literally infected the world. Although coronavirus spike proteins can recognize a broad range of host cell-surface proteins, inhibiting spike protein binding to a survival factor called GRP78 results in a significant reduction in SARS-CoV-2 attachment, entry and replication in lung and kidney cells. This inhibition is accomplished with a novel type of inhibitor that potently blocks the binding of SARS-CoV-2 spike protein and whole virus to surface-bound GRP78. These novel GRP78 inhibitors also down regulate cytokines (IL10, IL6), immune co-inhibitory checkpoint proteins (PD-L1, B7H3, B7H4), and up regulate immune co-stimulatory proteins (MHC-II, CD-86) resulting in the reduction of the immune suppressive nature of infected lung alveolar epithelial cells in vitro and in vivo. Finally, these novel GRP78 inhibitors inhibit the hyperfibrinolysis of infected lung cells by reducing the activation of plasmin on cell surfaces.

Abstract: Glucose-regulated protein (GRP78) antagonists that block, interfere, and/or inhibit binding of receptor tyrosine kinase orphan receptors (RORs) are described for use as immunotherapy anticancer. These GRP78 antagonists inhibit surface bound GRP78 binding and receptor signaling and are believed to mimic the behavior of anti-angiogenic kringles found in mammalian plasminogen and in receptor tyrosine kinase orphan receptors. These GRP78 antagonist may be free peptide fragments, or peptide fragments covalently fused to blood borne proteins such as albumin or immunoglobins, or modified peptide fragments that a designed to bind to blood or tissue peptides when introduced in vivo into the blood stream of a patient.

Abstract: Glucose-regulated protein (GRP78) antagonists that block, interfere, and/or inhibit binding of receptor tyrosine kinase orphan receptors (RORs) are described for use as as immunotherapy anticancer. These GRP78 antagonists inhibit surface bound GRP78 binding and receptor signaling and are believed to mimic the behavior of anti-angiogenic kringles found in mammalian plasminogen and in receptor tyrosine kinase orphan receptors. These GRP78 antagonist may be free peptide fragments, or peptide fragments covalently fused to blood borne proteins such as albumin or immunoglobins, or modified peptide fragments that a designed to bind to blood or tissue peptides when introduced in vivo into the blood stream of a patient.

Abstract: An intelligent firewall that prevents unauthorized access to a system has been developed. The fire wall does not use a communication address. It receives a data packet and analyzes it to determine its final disposition. Finally, the firewall handles the data packet according to its final disposition.

Abstract: Conjugated kringle protein fragments are disclosed as compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: An intelligent firewall that prevents unauthorized access to a system has been developed. The fire wall does not use a communication address. It receives a data packet and analyzes it to determine its final disposition. Finally, the firewall handles the data packet according to its final disposition.

Abstract: An intelligent firewall that prevents unauthorized access to a system has been developed. The fire wall does not use a communication address. It receives a data packet and analyzes it to determine its final disposition. Finally, the firewall handles the data packet according to its final disposition.

Abstract: Mammalian kringle 5 fragments and kringle 5 fusion proteins are disclosed as a compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: A method of processing data traffic at a firewall has been developed. The method prevents unauthorized access to a computer system by first receiving a SYN request for access to a destination in the system at a firewall. Upon receipt of a SYN request, the firewall sends a reply with an SYN/ACK message with changed packet information within the SYN/ACK message. The firewall receives an ACK message in reply to the SYN/ACK message. After the ACK message is authenticated by the firewall, the SYN request is recreated and forwarded to the destination in the system.

Abstract: Conjugated kringle protein fragments are disclosed as compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: A disc brake assembly includes a brake pad support member including a wall forming an aperture. A pad is at least partially disposed in the aperture. The pad is constructed from a friction material defining a front friction face and a back face opposite the front face. A perimeter is arranged between the faces. An insert is embedded the pad between the faces and preferably extends to the perimeter adjacent to the wall with the insert receiving the lateral load during braking. Preferably, the insert extends to the back face with a terminal portion of the insert flush with the back face for receiving a brake actuation load. The insert includes a protrusion that locates the insert relative to the friction material during the disc pad forming process. The brake actuator is supported by the brake pad support member for exerting a brake actuation load on the back face of the brake pad, preferably on the insert.

Abstract: Mammalian kringle 5 fragments and kringle 5 fusion proteins are disclosed as a compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: Conjugated kringle protein fragments are disclosed as compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: A disc brake assembly includes a brake pad support member including a wall forming an aperture. A pad is at least partially disposed in the aperture. The pad is constructed from a friction material defining a front friction face and a back face opposite the front face. A perimeter is arranged between the faces. An insert is embedded the pad between the faces and preferably extends to the perimeter adjacent to the wall with the insert receiving the lateral load during braking. Preferably, the insert extends to the back face with a terminal portion of the insert flush with the back face for receiving a brake actuation load. The insert includes a protrusion that locates the insert relative to the friction material during the disc pad forming process. The brake actuator is supported by the brake pad support member for exerting a brake actuation load on the back face of the brake pad, preferably on the insert.

Abstract: Mammalian kringle 5 fragments and kringle 5 fusion proteins are disclosed as a compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: The subject invention relates to uses of a receptor referred to as GRP78 and to other endothelial cell receptors which bind to the kringle 5 region of mammalian plasminogen. More specifically, identification of the functional properties of this receptor and other such receptors allows for the development and screening of agents which, for example, mimic K5 (i.e, mimetics) and therefore inhibit angiogenesis.

Abstract: Conjugated kringle protein fragments are disclosed as compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: Compounds having Formula I or pharmaceutically acceptable salts or prodrugs thereof, are useful for treating pathological states which arise from or are exacerbated by angiogenesis. The invention also relates to pharmaceutical compositions comprising these compounds and to methods of inhibiting angiogenesis in a mammal.

Abstract: Mammalian kringle 5 fragments are disclosed as a compounds for treating angiogenic diseases. Methods and compositions for inhibiting angiogenic diseases are also disclosed.

Abstract: Compounds having Formula I ##STR1## or pharmaceutically acceptable salts or prodrugs thereof, are useful for treating pathological states which arise from or are exacerbated by angiogenesis. The invention also relates to pharmaceutical compositions comprising these compounds and to methods of inhibiting anglogenesis in a mammal.