Abstract: The present disclosure relates to methods for detecting an increased risk of preeclampsia, determining the presence of preeclampsia, reducing the likelihood that preeclampsia will develop and treating preeclampsia. It also provides methods of measuring relaxin levels in a biological sample of a pregnant woman.

Abstract: The invention relates to the method for treatment, diagnosis and prevention of diseases related to fetal growth and placental insufficiency and comprises methods including inhibiting or increasing relaxin synthesis, relaxin receptor synthesis, relaxin binding to the relaxin receptor, and relaxin receptor activity. The invention also relates to screening assays to identify compounds that modulate relaxin and/or relaxin receptor activity. The invention further relates to gene therapy methods utilizing relaxin and relaxin-related sequences for the treatment and prevention of diseases related to fetal growth and placental insufficiency.

Abstract: The present invention concerns methods and compositions for making and using bioactive assemblies of defined compositions, which may have multiple functionalities and/or binding specificities. In particular embodiments, the bioactive assembly is formed using dock-and-lock (DNL) methodology, which takes advantage of the specific binding interaction between dimerization and docking domains (DDD) and anchoring domains (AD) to form the assembly. In various embodiments, one or more effectors may be attached to a DDD or AD sequence. Complementary AD or DDD sequences may be attached to an adaptor module that forms the core of the bioactive assembly, allowing formation of the assembly through the specific DDD/AD binding interactions. Such assemblies may be attached to a wide variety of effector moieties for treatment, detection and/or diagnosis of a disease, pathogen infection or other medical or veterinary condition.

Abstract: The disclosure pertains to methods of decreasing the risk of premature birth and miscarriage in human females. Particularly, the disclosure provides methods of reducing cervical dialation and preterm delivery by administration of relaxin.

Abstract: The present disclosure relates to methods for treating human subjects afflicted with chronic heart failure. The methods described herein employ administration of relaxin.

Abstract: Human relaxin analogs, polypeptide compositions related thereto, as well as nucleotide compositions encoding the same, are provided.

Abstract: Provided herein are modified relaxin polypeptides wherein the B chain comprises the core amino acid sequence CGR-XXX-R-XX-I/V-XX-CG (SEQ ID NO:1), where X is any amino acid. Also provided are modified relaxin polypeptides comprising at least an A and a B chain, wherein the A and B chains are derived from different naturally occurring relaxins and wherein the B chain comprises the core amino acid sequence CGR-XXX-R-XX-I/V-XX-CG (SEQ ID NO:1), where X is any amino acid.

Abstract: A process for producing an insulin type peptide, for example a relaxin, involving oxidizing a methionine residue on a B-chain having cysteine residues and combining the B chain with an A chain having cysteine residues to form a peptide having intermolecular disulphide links and biological activity. Novel synthetic relaxin 1 and methionine oxidized relaxins and Met(O) B-chains having enhanced solubility are disclosed.

Abstract: Human H3 preprorelaxin, human H3 prorelaxin, human H3 relaxin, human relaxin analogues having a modified A chain and/or a modified B chain are described. Also described are nucleic acid sequences encoded human H3 preprorelaxin, human H3 prorelaxin, human H3 relaxin, human relaxin analogues. Also described are methods for the treatment of conditions responsive to administration of H3 relaxin or analogues thereof.

Abstract: Modified H2 relaxms which act as antagonists of the relaxm receptor in cells and tissues, in particular, modified H2 relaxms comprising one or more alterations of the ammo acid sequence at positions B 13, B17 and B20 located in the receptor binding domain The antagonists retain affinity to the receptor, but do not substantially activate the receptor once bound thereto The H2 relaxm antagonists are used in compositions and methods for the treatment of cancers wherein a relaxm receptor is expressed