niclosamide has been researched along with Colorectal Cancer in 11 studies
Niclosamide: An antihelmintic that is active against most tapeworms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p48)
niclosamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of 5-chlorosalicylic acid with the amino group of 2-chloro-4-nitroaniline. It is an oral anthelmintic drug approved for use against tapeworm infections.
| Excerpt | Relevance | Reference |
|---|---|---|
| "The mechanistic role of niclosamide in CSC inhibition was examined in public databases, human colorectal cancer cells, colorectal cancer xenografts, and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colorectal cancer model." | 7.91 | Inhibition of LEF1-Mediated DCLK1 by Niclosamide Attenuates Colorectal Cancer Stemness. ( Baek, JH; Choi, JH; Kim, JH; Kim, JY; Lee, CJ; Nam, JS; Park, SY; Sarkar, S; Singh, P, 2019) |
| " Toxicities will be graded according to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v4." | 6.87 | Phase II trial to investigate the safety and efficacy of orally applied niclosamide in patients with metachronous or sychronous metastases of a colorectal cancer progressing after therapy: the NIKOLO trial. ( Burock, S; Daum, S; Keilholz, U; Neumann, K; Stein, U; Walther, W, 2018) |
| "Niclosamide reduces the growth of colorectal cancer cells by targeting several intracellular signalling pathways, including the β-catenin-dependent WNT signalling pathway." | 6.61 | New insights into niclosamide action: autophagy activation in colorectal cancer. ( Newton, PT, 2019) |
| " Further, encapsulation of NCS improved its effectiveness in vitro, particularly against colonspheres, and allowed to increase its intravenous dosage in vivo by increasing the amount of NCS able to be administered without causing toxicity." | 5.62 | Polymeric micelles targeted against CD44v6 receptor increase niclosamide efficacy against colorectal cancer stem cells and reduce circulating tumor cells in vivo. ( Abasolo, I; Andrade, F; Arango, D; Boullosa, A; Cámara-Sánchez, P; Díaz-Riascos, ZV; García-Aranda, N; Martínez-Trucharte, F; Montero, S; Nestor, M; Rafael, D; Sarmento, B; Schwartz, S; Seras-Franzoso, J; Vilar-Hernández, M, 2021) |
| "Niclosamide was found to inhibit expression and activation of STAT3 in a concentration- and time-dependent manner, thereby downregulating STAT3 downstream targets including survivin and cyclin-D1 to induce apoptosis and cell cycle arrest." | 5.56 | Repurposing of niclosamide as a STAT3 inhibitor to enhance the anticancer effect of chemotherapeutic drugs in treating colorectal cancer. ( Cho, WCS; To, KKW; Tong, CWS; Wu, MM; Yan, VW; Zhang, Z, 2020) |
| "Niclosamide treatment is associated with an inhibitory effect on CRC development and reduced Wnt activity." | 5.43 | The anthelmintic niclosamide inhibits colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling pathway. ( Bocuk, D; Klemm, F; Koenig, S; Krause, P; Monin, MB; Niebert, S; Pukrop, T; Stelling, R, 2016) |
| "The mechanistic role of niclosamide in CSC inhibition was examined in public databases, human colorectal cancer cells, colorectal cancer xenografts, and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colorectal cancer model." | 3.91 | Inhibition of LEF1-Mediated DCLK1 by Niclosamide Attenuates Colorectal Cancer Stemness. ( Baek, JH; Choi, JH; Kim, JH; Kim, JY; Lee, CJ; Nam, JS; Park, SY; Sarkar, S; Singh, P, 2019) |
| " Toxicities will be graded according to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v4." | 2.87 | Phase II trial to investigate the safety and efficacy of orally applied niclosamide in patients with metachronous or sychronous metastases of a colorectal cancer progressing after therapy: the NIKOLO trial. ( Burock, S; Daum, S; Keilholz, U; Neumann, K; Stein, U; Walther, W, 2018) |
| "Niclosamide reduces the growth of colorectal cancer cells by targeting several intracellular signalling pathways, including the β-catenin-dependent WNT signalling pathway." | 2.61 | New insights into niclosamide action: autophagy activation in colorectal cancer. ( Newton, PT, 2019) |
| " Further, encapsulation of NCS improved its effectiveness in vitro, particularly against colonspheres, and allowed to increase its intravenous dosage in vivo by increasing the amount of NCS able to be administered without causing toxicity." | 1.62 | Polymeric micelles targeted against CD44v6 receptor increase niclosamide efficacy against colorectal cancer stem cells and reduce circulating tumor cells in vivo. ( Abasolo, I; Andrade, F; Arango, D; Boullosa, A; Cámara-Sánchez, P; Díaz-Riascos, ZV; García-Aranda, N; Martínez-Trucharte, F; Montero, S; Nestor, M; Rafael, D; Sarmento, B; Schwartz, S; Seras-Franzoso, J; Vilar-Hernández, M, 2021) |
| "Niclosamide was found to inhibit expression and activation of STAT3 in a concentration- and time-dependent manner, thereby downregulating STAT3 downstream targets including survivin and cyclin-D1 to induce apoptosis and cell cycle arrest." | 1.56 | Repurposing of niclosamide as a STAT3 inhibitor to enhance the anticancer effect of chemotherapeutic drugs in treating colorectal cancer. ( Cho, WCS; To, KKW; Tong, CWS; Wu, MM; Yan, VW; Zhang, Z, 2020) |
| " Moreover, we found DK419 inhibited the growth of CRC tumor cells in vitro, had good plasma exposure when dosed orally, and inhibited the growth of patient derived CRC240 tumor explants in mice dosed orally." | 1.48 | Identification of DK419, a potent inhibitor of Wnt/β-catenin signaling and colorectal cancer growth. ( Chen, W; Hsu, D; Jing, G; Lu, M; Lyerly, HK; Mook, RA; Ren, XR; Spasojevic, I; Wang, J; Zhang, Q, 2018) |
| "Niclosamide treatment is associated with an inhibitory effect on CRC development and reduced Wnt activity." | 1.43 | The anthelmintic niclosamide inhibits colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling pathway. ( Bocuk, D; Klemm, F; Koenig, S; Krause, P; Monin, MB; Niebert, S; Pukrop, T; Stelling, R, 2016) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 8 (72.73) | 24.3611 |
| 2020's | 3 (27.27) | 2.80 |
| Authors | Studies |
|---|---|
| Wang, J | 2 |
| Mook, RA | 2 |
| Ren, XR | 2 |
| Zhang, Q | 1 |
| Jing, G | 1 |
| Lu, M | 1 |
| Spasojevic, I | 2 |
| Lyerly, HK | 3 |
| Hsu, D | 2 |
| Chen, W | 3 |
| Kortüm, B | 1 |
| Radhakrishnan, H | 1 |
| Zincke, F | 1 |
| Sachse, C | 1 |
| Burock, S | 2 |
| Keilholz, U | 2 |
| Dahlmann, M | 1 |
| Walther, W | 2 |
| Dittmar, G | 1 |
| Kobelt, D | 1 |
| Stein, U | 2 |
| Wu, MM | 1 |
| Zhang, Z | 1 |
| Tong, CWS | 1 |
| Yan, VW | 1 |
| Cho, WCS | 1 |
| To, KKW | 1 |
| Andrade, F | 1 |
| Rafael, D | 1 |
| Vilar-Hernández, M | 1 |
| Montero, S | 1 |
| Martínez-Trucharte, F | 1 |
| Seras-Franzoso, J | 1 |
| Díaz-Riascos, ZV | 1 |
| Boullosa, A | 1 |
| García-Aranda, N | 1 |
| Cámara-Sánchez, P | 1 |
| Arango, D | 1 |
| Nestor, M | 1 |
| Abasolo, I | 1 |
| Sarmento, B | 1 |
| Schwartz, S | 1 |
| Daum, S | 1 |
| Neumann, K | 1 |
| Park, SY | 1 |
| Kim, JY | 1 |
| Choi, JH | 1 |
| Kim, JH | 1 |
| Lee, CJ | 1 |
| Singh, P | 1 |
| Sarkar, S | 1 |
| Baek, JH | 1 |
| Nam, JS | 1 |
| Piao, H | 1 |
| Zhao, S | 1 |
| Osada, T | 2 |
| Premont, RT | 1 |
| Morse, MA | 2 |
| Newton, PT | 1 |
| Monin, MB | 1 |
| Krause, P | 1 |
| Stelling, R | 1 |
| Bocuk, D | 1 |
| Niebert, S | 1 |
| Klemm, F | 1 |
| Pukrop, T | 1 |
| Koenig, S | 1 |
| Cerles, O | 1 |
| Benoit, E | 1 |
| Chéreau, C | 1 |
| Chouzenoux, S | 1 |
| Morin, F | 1 |
| Guillaumot, MA | 1 |
| Coriat, R | 1 |
| Kavian, N | 1 |
| Loussier, T | 1 |
| Santulli, P | 1 |
| Marcellin, L | 1 |
| Saidu, NE | 1 |
| Weill, B | 1 |
| Batteux, F | 1 |
| Nicco, C | 1 |
| Chen, M | 1 |
| Yang, XY | 1 |
| Vandeusen, JB | 1 |
| Clary, BM | 1 |
| Clay, TM | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase II Trial to Investigate the Safety and Efficacy of Orally Applied Niclosamide in Patients With Metachronous or Synchronous Metastases of a Colorectal Cancer Progressing After Therapy[NCT02519582] | Phase 2 | 37 participants (Anticipated) | Interventional | 2015-08-31 | Recruiting | ||
| A Phase I Study of Niclosamide in Patients With Resectable Colon Cancer[NCT02687009] | Phase 1 | 1 participants (Actual) | Interventional | 2017-11-07 | Terminated (stopped due to low accrual) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for niclosamide and Colorectal Cancer
| Article | Year |
|---|---|
New insights into niclosamide action: autophagy activation in colorectal cancer.
Topics: Animals; Autophagic Cell Death; Colorectal Neoplasms; Humans; Neoplasm Metastasis; Niclosamide; Wnt | 2019 |
1 trial available for niclosamide and Colorectal Cancer
| Article | Year |
|---|---|
Phase II trial to investigate the safety and efficacy of orally applied niclosamide in patients with metachronous or sychronous metastases of a colorectal cancer progressing after therapy: the NIKOLO trial.
Topics: Administration, Oral; Adult; Aged; Colorectal Neoplasms; Female; Gene Expression Regulation, Neoplas | 2018 |
9 other studies available for niclosamide and Colorectal Cancer
| Article | Year |
|---|---|
Identification of DK419, a potent inhibitor of Wnt/β-catenin signaling and colorectal cancer growth.
Topics: Animals; Antineoplastic Agents; Benzimidazoles; beta Catenin; Cell Line, Tumor; Colorectal Neoplasms | 2018 |
Combinatorial treatment with statins and niclosamide prevents CRC dissemination by unhinging the MACC1-β-catenin-S100A4 axis of metastasis.
Topics: Amino Acids; beta Catenin; Colonic Neoplasms; Colorectal Neoplasms; Gene Expression Regulation, Neop | 2022 |
Repurposing of niclosamide as a STAT3 inhibitor to enhance the anticancer effect of chemotherapeutic drugs in treating colorectal cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Cell Cycle Checkpoints; Cell Line, Tumor; | 2020 |
Polymeric micelles targeted against CD44v6 receptor increase niclosamide efficacy against colorectal cancer stem cells and reduce circulating tumor cells in vivo.
Topics: Cell Line, Tumor; Colorectal Neoplasms; Humans; Hyaluronan Receptors; Micelles; Neoplastic Cells, Ci | 2021 |
Inhibition of LEF1-Mediated DCLK1 by Niclosamide Attenuates Colorectal Cancer Stemness.
Topics: Animals; Cell Line, Tumor; Cell Proliferation; Colorectal Neoplasms; Doublecortin-Like Kinases; Drug | 2019 |
Niclosamide-induced Wnt signaling inhibition in colorectal cancer is mediated by autophagy.
Topics: Autophagy; Autophagy-Related Protein-1 Homolog; beta Catenin; Colorectal Neoplasms; Dishevelled Prot | 2019 |
The anthelmintic niclosamide inhibits colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling pathway.
Topics: Adenocarcinoma; Animals; Antineoplastic Agents; beta Catenin; Biomarkers; Biomarkers, Tumor; Blottin | 2016 |
Niclosamide Inhibits Oxaliplatin Neurotoxicity while Improving Colorectal Cancer Therapeutic Response.
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Colorectal Neoplasms; Disease Model | 2017 |
Antihelminth compound niclosamide downregulates Wnt signaling and elicits antitumor responses in tumors with activating APC mutations.
Topics: Adaptor Proteins, Signal Transducing; Animals; Anthelmintics; Antineoplastic Agents; beta Catenin; C | 2011 |