COTI-2 hydrochloride
Based on 4 publication(s) in Google Scholar
COTI-2 hydrochloride is an orally active thiosemicarbazone anticancer agent and p53 mutant activator. COTI-2 hydrochloride induces Apoptosis. COTI-2 hydrochloride triggers the activation of AMPK and the inhibition of the mTOR pathway. COTI-2 hydrochloride induces DNA damage and replication stress responses. COTI-2 hydrochloride binds to misfolded mutant p53 proteins, thereby inducing conformational changes that restore p53 to its normal state and reactivate its function. COTI-2 hydrochloride acts on a variety of cancer cell lines and xenografts. COTI-2 hydrochloride can be used in research related to colorectal cancer, small cell lung cancer, glioblastoma, breast cancer, and ovarian cancer.
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- CAS. Nr.: 1204956-74-0
- Formel: C19H23ClN6S
- Molecular Weight:402.94
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) COTI-2 hydrochloride
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Biologische Aktivität
COTI-2 (72 h treatment) hydrochloride inhibits the proliferation of all tested cancer cell lines, including HEC-1A, Ovcar-8, KLE, HL-60, A549 and H226, with IC50 values ranging from near 0 nM to over 200 nM after 72 h of treatment[1].
COTI-2 (96 h treatment) hydrochloride potently inhibits the proliferation of colorectal cancer cell lines SW620, COLO-205 and HCT-15, as well as non-small cell lung cancer (NSCLC) cell lines H292 and H1975, and exhibits superior efficacy to Cetuximab (HY-P9905) or Erlotinib (HY-50896) after 96 h of treatment[1].
COTI-2 (4-7 days) hydrochloride inhibits the proliferation of U87-MG, SNB-19, SF-268 and SF-295 glioblastoma cell lines, with IC50 values in the nanomolar range; after 4-7 days of treatment, its potency against U87-MG and SNB-19 cell lines is 10 to 500-fold that of Cisplatin (HY-17394) and BCNU (HY-13585)[1].
COTI-2 (100-1000 nM; 48 h) hydrochloride induces apoptosis in small cell lung cancer SHP-77 cells. Specifically, treatment with IC50 concentrations (100 nM, 250 nM) for 48 h results in early apoptosis in 40.13% to 46.68% of cells, while treatment with the IC90 concentration (1000 nM) for 48 h induces early apoptosis as well as late apoptosis/necrosis in most cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Diverse human cancer cell lines including small cell lung cancer (SCLC), non-small cell lung cancer (NSCLC), colorectal, glioma/astrocytoma, ovarian carcinoma, breast, leukemia, endometrial, and pancreatic cancer cell lines (HEC-1A, Ovcar-8, KLE, HL-60, A549, H226)
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Concentration:Multiple concentrations
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Incubation Time:72 h
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Result:Efficiently inhibited the proliferation rate of all tested cell lines.
Showed nanomolar sensitivity in most cell lines, with IC50 values ranging from near 0 nM to over 200 nM.
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Cell Line:Human glioblastoma cell lines (U87-MG, SNB-19, SF-268, SF-295)
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Concentration:Multiple concentrations
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Incubation Time:4-7 days
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Result:Was active against all tested glioblastoma cell lines at relatively low concentrations.
Showed superior activity and lower nanomolar IC50 values compared to cisplatin and BCNU in U87-MG and SNB-19 cell lines, being 10 to 500 times more effective than these agents.
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Cell Line:SHP-77 human small cell lung cancer (SCLC) cells
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Concentration:100 nM, 250 nM, 1000 nM
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Incubation Time:48 h
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Result:Induced early apoptosis in 40.13% to 46.68% of total cells at IC50 concentrations (100 nM, 250 nM).
Induced early apoptosis in 17.15% and late apoptosis/necrosis in 19.25% of total cells, with 13.64% of cells undergoing necrosis, at IC90 concentration (1000 nM).
COTI-2 (3 mg/kg; i.p.; once every two days; up to 38 days) hydrochloride effectively inhibits the growth of SHP-77 small cell lung cancer xenografts, and exhibits superior efficacy compared with standard chemotherapy compounds[1].
COTI-2 (8 mg/kg; intraperitoneal injection; three times per week) hydrochloride doubles the time required for U87-MG glioblastoma xenografts to reach the target tumor volume, and significantly delays tumor growth[1].
COTI-2 (200 mg/kg; p.o.; 5 days per week) hydrochloride significantly inhibits the growth of MDA-MB-231 breast cancer xenografts[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NCr-nu mice (immunocompromised, n=5 per group)[1]
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Dosage:10 mg/kg
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Administration:i.p.; 5 days a week; 7 weeks
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Result:Significantly reduced tumor volumes at multiple time points post-treatment.
Increased the time for tumors to reach a mean volume of ~620 mm3 from 32 days to 48 days, a 50% increase compared to controls.
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Animal Model:NCr-nu mice (immunocompromised, n=5 per group)[1]
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Dosage:3 mg/kg
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Administration:i.p.; once every two days; up to 38 days
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Result:Significantly inhibited SHP-77 xenograft growth to a greater degree than cisplatin or paclitaxel.
Maintained treated tumors at a minimal volume (~10 mm3 or less) through 38 days, while control tumors reached ~260 mm3.
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Animal Model:Nude mice (immunocompromised, 7 mice per group)[1]
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Dosage:8 mg/kg
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Administration:i.p.; 3 times per week
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Result:Significantly reduced tumor volumes at multiple time points.
Doubled the time for tumors to reach a mean volume of ~840 mm3 from 5 days to 10 days compared to controls.
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Animal Model:SCID mice (immunocompromised, 7 mice per group, 6-8 weeks old)[1]
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Dosage:200 mg/kg
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Administration:p.o.; 5 days per week
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Result:Significantly delayed MDA-MB-231 xenograft growth compared to vehicle controls.
Chemical Information
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CAS. Nr. 1204956-74-0
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Molecular Weight 402.94
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Formel C19H23ClN6S
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SMILES
S=C(N1CCN(CC1)C2=NC=CC=C2)N/N=C3C4=NC=CC=C4CCC/3.Cl
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Cell Death Dis
2023 Dec 14;14(12):831. PMID: 38097548 -
Cell Rep
Repurposing antiparasitic antimonials to noncovalently rescue temperature-sensitive p53 mutations. [Abstract]2022 Apr 12;39(2):110622. PMID: 35417717 -
Int J Mol Sci
Improving Reporter Gene Assay Methodology for Evaluating the Ability of Compounds to Restore P53 Activity. [Abstract]2022 Nov 10;23(22):13867. PMID: 36430341 -
Iran J Basic Med Sci
COTI-2 suppresses the malignancy of bladder cancer by inducing apoptosis via the AMPK-mTOR signaling pathway. [Abstract]2025;28(3):240-246. PMID: 39906622
Reinheit & Dokumentation
Verweise
[1]. Salim KY, et al. COTI-2, a novel small molecule that is active against multiple human cancer cell lines in vitro and in vivo. Oncotarget. 2016 Jul 05;7(27):41363-41379. [Content Brief]
[2]. Duffy MJ, et al. Mutant p53 as a target for cancer treatment. Eur J Cancer. 2017 Sep;83:258-265. [Content Brief]
[3]. Lindemann A, et al. COTI-2, A Novel Thiosemicarbazone Derivative, Exhibits Antitumor Activity in HNSCC through p53-dependent and -independent Mechanisms. Clin Cancer Res. 2019 Sep 15;25(18):5650-5662. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
COTI-2 hydrochloride Related Classifications
HY-19896A Related Classifications
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