Antimalarial agent 49
Antimalarial agent 49 is an orally active antimalarial compound. Antimalarial agent 49 inhibits growth of Pf3D7 and PfK1 strains (IC50: 0.84 μM and 0.4 μM respectively). Antimalarial agent 49 has antimalarial activity and inhibits the development of P. berghei liver stages. Antimalarial agent 49 can be used in the study of Plasmodium infection.
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- 화학식: C28H18F4N6O
- 분자량:530.48
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Parasite Isoforms
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Biological Activity
제품 설명
In Vitro
Antimalarial agent 49 (compound 15k) (0.37-10 μM, 40 h) inhibits the development of P. berghei liver stage (IC50: 5.88 μM)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | T1/2 | Tmax | Plasma Concentration | Vd | Clearance (CL) | AUC | MRT |
|---|---|---|---|---|---|---|---|---|---|
| Mice[1] | 100 mg/kg | p.o. | 3.74 h | 4.00 h | 15.17 ng/mL | 4.97 L/kg | 0.92 L/h/kg | 0.11 ng·h/mL | 7.30 h |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Female Swiss mice (6-8-week-old, 18 ± 2 g) were intra-peritoneally inoculated with 1x106 P.yoelii N67 infected red blood cells (iRBCs)[1]
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Dosage:100 mg/kg
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Administration:Oral gavage (p.o.), once every day for 4 d
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Result:Inhibited 42.55% of parasite growth on the 7th day and 35.93% of parasite growth on the 10th day.
Prolonged the median survival time (17 d) compared with the Chloroquine (HY-17589A) (10 mg/kg)-treated group (16 d).
Chemical Information
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분자량 530.48
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화학식 C28H18F4N6O
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SMILES
O=C(C1=CC2=C(C(C3=CC=C(F)C=C3)=N1)NC4=C2C=CC=C4)NCC5=CN(C6=CC=CC(C(F)(F)F)=C6)N=N5
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)