Drug intelligence / Profile preview

ADH-1 + capecitabine

Development stage
Unknown
Lead developer
Fennec Pharmaceuticals
Modality
Orthosteric Ligands → Classical Binding Small Molecules → Small Molecules, Peptides, Metabolically Activated Prodrugs → Prodrugs/Conditional Activator Small Molecules → Small Molecules, Covalent Small Molecules → Small Molecules, Nucleic Acid-Directed Small Molecules → Small Molecules
Administration
Intravenous, Oral
01

Overview

ADH-1 + capecitabine is a combination therapy under investigation for cancer treatment. ADH-1 is a synthetic cyclic pentapeptide that selectively and competitively binds to and blocks N-cadherin, a cell adhesion molecule present on certain tumor cells and tumor vasculature. By inhibiting N-cadherin, ADH-1 disrupts cadherin-mediated signaling pathways essential for tumor cell survival and induces apoptosis (cell death) in cancer cells. It also causes disruption of the blood vessels supplying tumors (angiolysis), further impairing tumor growth[6]. Capecitabine is an orally administered prodrug of 5-fluorouracil (5-FU), classified as an antimetabolite chemotherapy agent. After absorption, it is converted into 5-FU preferentially within tumor tissues by enzymatic processes, where it inhibits thymidylate synthase and interferes with DNA synthesis in rapidly dividing cancer cells[4][5]. The combination aims to exploit complementary mechanisms—targeted disruption of cell adhesion/tumor vasculature by ADH-1 with cytotoxic antimetabolite activity from capecitabine.

02

Targets

CDH2 (N-cadherin)TS (Thymidylate synthase)

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