8 results about "Cystine knot" patented technology

Provided herein are compounds of Formulae (I'), (I), (IV'), and (IV). Also provided herein are methods of preparation of Formulae (Ill-i), (VI), and (VIII). Further provided herein are methods of functionalizing or sequencing a peptide having at least one free cysteine residue, and methods of enriching a sample comprising one or more peptides.

The present application relates to a protein dimer formed from a first fusion protein and a second fusion protein, wherein the first fusion protein comprises a cystine knot domain (CK) fused to a first pharmaceutically active protein and the second fusion protein comprises a CK domain fused to a second pharmaceutically active protein, wherein the two fusion proteins are covalently linked via their CK domains. The present application further relates to the individual fusion proteins, polynucleotides encoding the fusion proteins, vectors comprising the polynucleotides, and host cells comprising the vectors.

The application relates to a protein dimer formed by a first and a second fusion protein, wherein the first fusion protein comprises a cystine knot domain (CK) fused to a first pharmaceutically active protein and the second fusion protein comprises a CK domain fused to a second pharmaceutically active protein, wherein the two fusion proteins are covalently linked by their CK domains. The application further relates to the individual fusion proteins, to the polynucleotide encoding the fusion proteins, the vector comprising the polynucleotide and the host cell comprising the vector.

The invention provides a polypeptide capable of inhibiting activated KRAS protein in a broad spectrum mode, the polypeptide comprises a KRAS targeting structural domain, and the KRAS targeting structural domain is an RAS binding structural domain (RBD)-cysteine-rich structural domain (CRD) of RAF1, an RBD structural domain of RAF1 or an RBD structural domain of SIN1. The invention further provides a combined administration method for broad-spectrum inhibition of multiple KRAS mutation tumors. The method disclosed by the invention can be used for treating various KRAS mutant tumors, and compared with a single micromolecular anticancer drug, the tumor inhibition effect can be remarkably improved.

The present invention relates to a grafted cyclotide comprising a cyclic cystine knot (CCK) derived from kalata B1 (kB1) and an amino acid sequence derived from dynorphin A (dynA sequence) grafted into the the inter-cysteine loop 3, 5 or 6 of said CCK. The present invention further relates to a pharmaceutical composition comprising the grafted cyclotide according to the invention. The present invention further relates to the grafted cyclotide or the pharmaceutical composition according to the invention for use in the treatment, amelioration or prophylaxis of a KOR-related disease, in particular of a disease resulting from or coming along with a decreased KOR activity and / or which is treatable by KOR agonism / an increased KOR activity. The present invention further relates to a method of preparing the grafted cyclotide according to the invention, namely the 'plug and play' synthesis approach of the invention. The present invention also relates to 'plug and play'-produced kB1-derived grafted cyclotides with loop 3-, loop 5- or loop 6- inserted dynA-derived grafts. The present invention further relates to the the disclosed kB1-derived acyclic grafting scaffold; as well as to the (linear) (kB1-derived) peptide backbone as comprised therein.

The present invention provides non-naturally occurring cystine nodules (CKPs) that bind to VEGF-A. In addition, methods of using non-naturally occurring CKPs that bind to VEGF-A are provided, including diagnostic and therapeutic compositions and methods. Non-natural CKPs that bind low density lipoprotein receptor associated protein 6 (LRP6) are also provided.