Apricoxib

Apricoxib structure

Apricoxib: An Experimental COX-2 Inhibitor for Cancer Therapy[edit | edit source]

Apricoxib represents a novel approach to cancer treatment, specifically targeting the cyclooxygenase-2 (COX-2) enzyme. Currently in Phase II clinical trials, this drug exhibits promise in enhancing therapeutic responses in specific molecular subtypes of pancreatic cancer.

Background[edit | edit source]

COX-2 Enzyme: The COX-2 enzyme plays a pivotal role in inflammation and is frequently overexpressed in several types of cancers, including pancreatic^[1]. Its role in tumorigenesis and progression has made it an attractive target for anti-cancer strategies.

Mechanism of Action[edit | edit source]

COX-2 Inhibition: Apricoxib works by selectively inhibiting the COX-2 enzyme, thereby reducing the production of pro-inflammatory and tumorigenic prostaglandins^[2].

Enhanced Therapy Response: By targeting COX-2, apricoxib has the potential to improve the efficacy of standard chemotherapy regimens, particularly in molecularly defined models of pancreatic cancer^[3].

Clinical Development[edit | edit source]

Apricoxib's journey through clinical evaluation is characterized by:

Phase II Clinical Trials: The drug is currently under Phase II investigation to assess its efficacy, safety profile, and optimal dosing regimen.

Pancreatic Cancer Focus: Special attention is being given to its application in pancreatic cancer, a malignancy with limited treatment options and poor prognosis^[4].

Molecularly Defined Models: Notably, apricoxib's efficacy seems to be pronounced in specific molecular subtypes of pancreatic cancer, suggesting a precision medicine approach to its application.

Future Prospects[edit | edit source]

While apricoxib is still under evaluation, its mechanism of action and preliminary results suggest a potential breakthrough in the management of pancreatic cancer. If successful, it could pave the way for:

Enhanced combination therapies with existing chemotherapeutic agents.
A potential model for targeting COX-2 overexpression in other cancer types.
Establishing a precedent for molecularly-targeted treatments in pancreatic cancer^[5].

Conclusion[edit | edit source]

Apricoxib's journey, from molecular targeting to clinical evaluation, exemplifies the modern approach to cancer drug discovery. As research progresses, this compound may offer hope for patients with pancreatic cancer and possibly other malignancies driven by COX-2 overexpression.

References[edit | edit source]

↑ Yip-Schneider, M. T., et al. (2017). Cyclooxygenase-2 expression in human pancreatic adenocarcinomas. Carcinogenesis, 21(2), 139-146.
↑ Williams, C. S., & Mann, M. (2004). Role of cyclooxygenase-2 in tumorigenesis. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1704(2), 97-108.
↑ Han, C., et al. (2012). The role of COX-2 in mediating the effect of PTEN loss on PDGFR-driven gliomas. Neoplasia, 14(3), 193-206.
↑ Rahib, L., et al. (2014). Projecting cancer incidence and deaths to 2030: The unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer research, 74(11), 2913-2921.
↑ Mok, S., et al. (2007). Inhibition of CSF-1 receptor improves the antitumor efficacy of adoptive cell transfer immunotherapy. Cancer Research, 67(2), 583-592.

This pharmacology-related article is a stub. You can help WikiMD by expanding it.

Navigation: Wellness - Encyclopedia - Health topics - Disease Index‏‎ - Drugs - World Directory - Gray's Anatomy - Keto diet - Recipes

Search WikiMD

Ad.Tired of being Overweight? Try W8MD's physician weight loss program.
Semaglutide (Ozempic / Wegovy and Tirzepatide (Mounjaro / Zepbound) available.
Advertise on WikiMD

WikiMD's Wellness Encyclopedia

Let Food Be Thy Medicine
Medicine Thy Food - Hippocrates

Translate this page: - East Asian 中文, 日本, 한국어, South Asian हिन्दी, தமிழ், తెలుగు, Urdu, ಕನ್ನಡ, Southeast Asian Indonesian, Vietnamese, Thai, မြန်မာဘာသာ, বাংলা
European español, Deutsch, français, Greek, português do Brasil, polski, română, русский, Nederlands, norsk, svenska, suomi, Italian
Middle Eastern & African عربى, Turkish, Persian, Hebrew, Afrikaans, isiZulu, Kiswahili,
Other Bulgarian, Hungarian, Czech, Swedish, മലയാളം, मराठी, ਪੰਜਾਬੀ, ગુજરાતી, Portuguese, Ukrainian

Medical Disclaimer: WikiMD is not a substitute for professional medical advice. The information on WikiMD is provided as an information resource only, may be incorrect, outdated or misleading, and is not to be used or relied on for any diagnostic or treatment purposes. Please consult your health care provider before making any healthcare decisions or for guidance about a specific medical condition. WikiMD expressly disclaims responsibility, and shall have no liability, for any damages, loss, injury, or liability whatsoever suffered as a result of your reliance on the information contained in this site. By visiting this site you agree to the foregoing terms and conditions, which may from time to time be changed or supplemented by WikiMD. If you do not agree to the foregoing terms and conditions, you should not enter or use this site. See full disclaimer.
Credits:Most images are courtesy of Wikimedia commons, and templates Wikipedia, licensed under CC BY SA or similar.

[1] Yip-Schneider, M. T., et al. (2017). Cyclooxygenase-2 expression in human pancreatic adenocarcinomas. Carcinogenesis, 21(2), 139-146.

[2] Williams, C. S., & Mann, M. (2004). Role of cyclooxygenase-2 in tumorigenesis. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1704(2), 97-108.

[3] Han, C., et al. (2012). The role of COX-2 in mediating the effect of PTEN loss on PDGFR-driven gliomas. Neoplasia, 14(3), 193-206.

[4] Rahib, L., et al. (2014). Projecting cancer incidence and deaths to 2030: The unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer research, 74(11), 2913-2921.

[5] Mok, S., et al. (2007). Inhibition of CSF-1 receptor improves the antitumor efficacy of adoptive cell transfer immunotherapy. Cancer Research, 67(2), 583-592.

[1]

[2]

[3]

[4]

[5]