AR-67

Target: Recurrent Glioblastoma Multiforme (reGBM), Colorectal, Ovarian, Pancreatic Cancer and Non-Small Cell Lung Carcinoma (NSCLC)

Third-generation, completely synthetic Camptothecin-based compound

Target: Recurrent Glioblastoma Multiforme (reGBM), Colorectal, Ovarian, Pancreatic Cancer and Non-Small Cell Lung Carcinoma (NSCLC)

Vivacitas’ lead development candidate (AR-67) is a third-generation, completely synthetic Camptothecin-based compound. Employing a proprietary synthesis method, AR-67 is a novel lipophilic compound which targets improved efficacy, tolerability, and stability.

New generation of treatment

AR-67 is a silatecan-based, 3rd generation camptothecin with chemical modifications that enhance blood stability and increase the likelihood of cell penetration.

Increased potency

AR-67 is highly lipophilic, meaning that it is readily taken up by the hydrophobic environment of cellular membranes, thus providing significant protection from the extracellular milieu where it would otherwise be broken down to its inactive form.

AR-67 has also demonstrated evidence of crossing the brain-blood barrier, in preclinical and Phase II clinical studies.

Creating a new path forward

AR-67 has shown promise in in vitro, Phase I, and Phase II studies for multiple tumor types and has demonstrated the potential for progression-free survival in patients with recurrent glioblastoma of 6-29 months while significantly reducing severe side effects normally associated with this drug class (e.g., grade 4 diarrhea).

Our Difference

References

1. Novel silatecan displays high lipophilicity, improved blood stability and potent
anticancer activity. Bom D, et al J Med Chem 2000; 43:3970-3980

2. Silatecan DB-67 is a novel DNA Topo-1 targeted radiation sensitizer: Chen AY. Mol
Cancer Ther 2005; 4(2): 317-24.

3. Phase I study publication: Arnold SM, et al. Clin Cancer Res. 2010;6:673-680

4. Phase II study publication (abstract): Kumthekar P, et al. SNO 2019. Poster ACTR-40,
published in Neuro-Oncology(https://academic.oup.com/neuro-oncology)

5. Ubiquitin-dependent Destruction of Topoisomerase I Is
Stimulated by the Antitumor Drug Camptothecin*, Desai et al. The Journal of Biological Chemistry, Vol. 272, No. 39, Issue of September 26, pp. 24159–24164, 1997.  https://www.jbc.org

6. Metabolic Pathways of the Camptothecin Analog AR-67, Horn et al. Drug Metabolism and Disposition, Vol. 39, No. 4, 37390/3672838, 2011. https://dmd.aspetjournals.org