 | |
| Company type | Private |
|---|---|
| Industry | Biotechnology |
| Founded | 2017 |
| Founder | Jef K. De Brabander, Jerry W. Shay |
| Headquarters | , |
Key people | Frank Perabo |
| Products | TASIN, THIO |
| Website | https://barricadetherapeutics.com/ |
Barricade Therapeutics, Corp. is a privately held Biotech company based in Houston & Dallas, TX and it was founded based on discovery and advancement of novel first in class small molecules, by integrating complex molecule synthesis, chemistry, and molecular pharmacology with targeted therapeutic approaches in cancer biology. The company focuses on the development of uniquely innovative targeted drugs for the treatment of patients with cancer and it is currently at the nonclinical stage of the development.
History
editBarricade Therapeutics is co-founded by a team of scientists and management experts in 2017. The founding scientists include Jef K. De Brabander, PhD, Jerry W. Shay, PhD and Deepak Nijhawan MD, PhD. The founding management team include Frank Perabo, MD PhD, Neil Thapar, PharmD, RPh and Vlad Vitoc, MD, MBA.
Nobel Drugs
editJef De Brabander, Ph.D. and Jerry W. Shay, Ph.D., at the University of Texas Southwestern, Medical Center, Dallas, TX. discovered the two nobel drugs, namely TASIN and THIO.
TASIN is a unique, first-in-class compound with a mechanism of action targeting truncated APC (adenomatous polyposis coli), one of the earliest and most critical mutations occurring in colorectal cancer (CRC). Truncated APC has a dominant role in CRC initiation and cancer progression and is expressed in >80% of those CRC tumors. Extensive preclinical work on TASIN demonstrates highly potent and selective targeting of truncated APC, resulting in significant inhibition of CRC tumor growth with no apparent toxicity to normal cells.[1][2][3]
THIO specifically targets tumorcell DNA and causes damage to DNA ends (telomeres), resulting in the selective death of tumor cells. This approach targets an almost universal driver of tumor growth and is supported by extensive preclinical work showing very significant antitumor activity across a broad range of tumors refractory to I/O-, BRAF-, EGFR-targeted therapies, as well as chemotherapy. Currently, patients failing these treatments have a poor prognosis and few alternative treatment options. THIO utilizes a novel mechanism of action, which successfully circumvents those resistance mechanisms, without relevant toxicity.[4][5][6][7][8][9]
Development Pipline
editBoth TASIN and THIO are currently at the non-clinical development stage.
Funding
editSeed funding of xxx amount was received
See Also
editReferences
edit- ^ Zhang, Lu; Theodoropoulos, Panayotis C.; Eskiocak, Ugur; Wang, Wentian; Moon, Young-Ah; Posner, Bruce; Williams, Noelle S.; Wright, Woodring E.; Kim, Sang Bum (10 19, 2016). "Selective targeting of mutant adenomatous polyposis coli (APC) in colorectal cancer". Science Translational Medicine. 8 (361): 361ra140. doi:10.1126/scitranslmed.aaf8127. ISSN 1946-6242. PMID 27798265.
{{cite journal}}: Check date values in:|date=(help) - ^ Cully, Megan (2016-11-29). "Anticancer drugs: Exploiting a weakness in colorectal cancers". Nature Reviews. Drug Discovery. 15 (12): 820–821. doi:10.1038/nrd.2016.247. ISSN 1474-1784. PMID 27895333.
- ^ Zhang, Lu; Shay, Jerry W. (08 01, 2017). "Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer". Journal of the National Cancer Institute. 109 (8). doi:10.1093/jnci/djw332. ISSN 1460-2105. PMID 28423402.
{{cite journal}}: Check date values in:|date=(help) - ^ Reyes-Uribe, Patricia; Adrianzen-Ruesta, Maria Paz; Deng, Zhong; Echevarria-Vargas, Ileabett; Mender, Ilgen; Saheb, Steven; Liu, Qin; Altieri, Dario C.; Murphy, Maureen E. (2018-04-26). "Exploiting TERT dependency as a therapeutic strategy for NRAS-mutant melanoma". Oncogene. doi:10.1038/s41388-018-0247-7. ISSN 1476-5594. PMID 29695835.
- ^ Sengupta, Satarupa; Sobo, Matthew; Lee, Kyungwoo; Senthil Kumar, Shiva; White, Angela R.; Mender, Ilgen; Fuller, Christine; Chow, Lionel Ml; Fouladi, Maryam (2018-04-13). "Induced Telomere Damage to Treat Telomerase Expressing Therapy-Resistant Pediatric Brain Tumors". Molecular Cancer Therapeutics. doi:10.1158/1535-7163.MCT-17-0792. ISSN 1538-8514. PMID 29654065.
- ^ Zhang, Gao; Wu, Lawrence W.; Mender, Ilgen; Barzily-Rokni, Michal; Hammond, Marc R.; Ope, Omotayo; Cheng, Chaoran; Vasilopoulos, Themistoklis; Randell, Sergio (2018-03-21). "Induction of Telomere Dysfunction Prolongs Disease Control of Therapy-Resistant Melanoma". Clinical Cancer Research: An Official Journal of the American Association for Cancer Research. doi:10.1158/1078-0432.CCR-17-2773. ISSN 1078-0432. PMID 29563139.
- ^ Mender, Ilgen; Gryaznov, Sergei; Dikmen, Z. Gunnur; Wright, Woodring E.; Shay, Jerry W. (2015-1). "Induction of telomere dysfunction mediated by the telomerase substrate precursor 6-thio-2'-deoxyguanosine". Cancer Discovery. 5 (1): 82–95. doi:10.1158/2159-8290.CD-14-0609. ISSN 2159-8290. PMC 4293221. PMID 25516420.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ Mender, Ilgen; Gryaznov, Sergei; Shay, Jerry W. (2015). "A novel telomerase substrate precursor rapidly induces telomere dysfunction in telomerase positive cancer cells but not telomerase silent normal cells". Oncoscience. 2 (8): 693–695. doi:10.18632/oncoscience.213. ISSN 2331-4737. PMC 4580061. PMID 26425659.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Shay, Jerry W. (06 2016). "Role of Telomeres and Telomerase in Aging and Cancer". Cancer Discovery. 6 (6): 584–593. doi:10.1158/2159-8290.CD-16-0062. ISSN 2159-8290. PMC 4893918. PMID 27029895.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link)