—US Food and Drug Administration (FDA)
At VenatoRx, we are pursuing novel chemical approaches to treat bacterial and viral infections. All of our investigational molecules were discovered internally.
Over many decades, bacteria have developed resistance to beta-lactam (BL) antibiotics by producing enzymes called beta-lactamases, which attack and destroy BL antibiotics. Today, over 70% of hospital based infections caused by gram-negative bacteria are associated with an antibiotic resistant organism.1 To overcome this resistance, BL antibiotics have been combined with protective beta-lactamase inhibitors (BLI). Unfortunately, existing BLIs are not sufficiently effective against the rapidly emerging extended spectrum beta-lactamases (ESBLs) and carbapenem-hydrolyzing beta-lactamases (carbapenemases). In addition, there are no approved BL based antibiotics that work against the metallo-beta-lactamase-producing superbugs carrying NDM or VIM.
Our lead agent, VNRX-5133, is a unique non-beta-lactam BLI with potent and selective activity against both serine- and metallo-beta-lactamases. VNRX-5133, in a fixed combination with the 4th generation cephalosporin Cefepime, has the potential to provide a best-in-class broad-spectrum treatment option for infections caused by:
- multi-drug resistant (MDR) gram-negative bacteria, including carbapenem-resistant
Enterobacteriaceae (CRE) and Pseudomonas aeruginosa (CRPA)
- suspected polymicrobial infections caused by both gram-negative and gram-positive
- bioterror pathogens such as Burkholderia spp. and Salmonella engineerable with metallo-
In addition to our BLI programs, we are developing a radically new class of antibiotic. BL antibiotics, which include the highly successful penicillins, cephalosporins, monobactams, and carbapenems, all kill bacteria by blocking a key enzyme involved in cell wall synthesis: the penicillin binding protein (PBP). Our novel PBP inhibitors represent a new class of non-beta-lactam molecules that kill bacteria by this same mechanism. But because they are chemically distinct from the BLs, they are not susceptible to beta-lactamases. If successful, our PBP inhibitors have the potential to revolutionize treatment of MDR bacterial infections and set the resistance clock back by decades.