Antiparasitic agent-15
Antiparasitic agent-15, a pyridine-thiazolidinone, has anti-Trypanosoma cruzi and leishmanicidal activities. Antiparasitic agent-15 has IC50s of 0.9 μM and 0.64 μM against trypomastigote and amastigote forms of T. cruzi. Antiparasitic agent-15 has IC50s of 42.2 μM and 9.58 μM against trypomastigote and amastigote forms of L. amazonensis. Antiparasitic agent-15 induces parasite cell death through necrosis induction. Antiparasitic agent-15 induces morphological changes such as shortening, retraction and curvature of the parasite body and leakage of internal content with T. cruzi trypomastigotes.
For research use only. We do not sell to patients.
- CAS No.: 3046451-91-3
- Formula: C17H16N4OS
- Molecular Weight:324.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Parasite Isoforms
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Biological Activity
Description
IC50 & Target
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Trypanosoma |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| RAW264.7 | CC50 |
146.1 μM
Compound: 18
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Cytotoxicity against mouse RAW264.7 cells incubated for 48 hrs by MTT assay
Cytotoxicity against mouse RAW264.7 cells incubated for 48 hrs by MTT assay
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[PMID: 37062170] |
In Vitro
Antiparasitic agent-15 (compound 18) has a CC50 of 146.1 μM in RAW 264.7[1].
Antiparasitic agent-15 (0.9, 1.8 μM; 24 h) promotes morphological changes such as shortening, retraction and curvature of the parasite body in trypomastigotes forms of T. cruzi. Antiparasitic agent-15 dose-independently induces significant alterations compatible with apoptosis in trypomastigotes[1].
Antiparasitic agent-15 (10 μg/mL; 24 h, 48 h, 72 h, and 96 h) causes a significant reduction in IL-10 production and an increase in IL-6 in supernatants of stimulated murine splenocytes[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3046451-91-3
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Molecular Weight 324.40
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Formula C17H16N4OS
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SMILES
CC1(S/C(N(C1=O)C2=CC=CC=C2)=N/N=C/C3=CC=CC=N3)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)