chikungunya

EIDD-1931 (Beta-d-N4-hydroxycytidine) 是一种核苷类抗病毒试剂 ，可抑制丙型肝炎病毒、基孔肯亚病毒和委内瑞拉马脑炎病毒的复制活性。

CHIKV-IN-2 基孔肯雅病毒的选择性抑制剂，具有强大的细胞抗病毒活性 (EC90=270 nM) 以及能够改善肝微粒体稳定性。它能够抑制细胞靶二氢乳清酸脱氢酶的活性。

Anti-Chikungunya virus E2 Antibody (CHK-265) 为针对 chikungunya virus E2 glycoprotein B domain 的小鼠来源IgG2c 类型抗体。其同型对照抗体为 Mouse IgG2c kappa, Isotype Control。

Cletoquine 是 Hydroxychloroquine 的主要活性代谢物。 Cletoquine 具有对抗基孔肯雅病毒 (CHIKV) 的能力。 Cletoquine 具有抗疟作用，并具有治疗自身免疫性疾病的潜力。

Cletoquine oxalate (Desethylhydroxychloroquine oxalate) is a major active metabolite of Hydroxychloroquine. Cletoquine has the ability to against the chikungunya virus (CHIKV). Cletoquine has antimalarial effects and has the potential for autoimmune disea

Cletoquine hydrochloride 是 Hydroxychloroquine 的主要活性代谢产物。Cletoquine hydrochloride 也是一种 Chloroquine 衍生物，具有抗基孔肯雅热病毒 (CHIKV) 的能力。Cletoquine hydrochloride 具有抗疟作用。

CHIKV nsP2 protease-IN-1 (compound J13) 是一种针对非结构蛋白2蛋白酶 (non-structural protein 2 protease) 的口服抑制剂，其对CH S27的EC50值为0.39 μM。该化合物可用于研究基孔肯雅病毒。

nsP2 Protease-IN-1 是一种针对 Chikungunya (CHIKV) 病毒nsP2半胱氨酸蛋白酶的高效不可逆共价抑制剂，IC50为60 nM。该化合物具有出色的抗阿尔法病毒活性，能够有效抑制 CHIKV 和 VEEV 的病毒复制，其 EC50 值分别为0.01 µM 和 0.3 µM。

NHC-diphosphate is an active phosphorylated intracellular metabolite of β-d-N4-Hydroxycytidine (NHC) as a diphosphate form[1]. NHC is a pyrimidine ribonucleoside and behaves as a potent anti-virus agent. NHC effectively inhibits the replication of venezuelan equine encephalitis virus (VEEV), Chikungunya virus (CHIKV) and hepatitis C virus (HCV)[1]. Huh-7 cells are incubated with (10-50 μM; 4 h) NHC or a McGuigan phosphoramidate prodrug of NHC.Intracellular levels of the parental compounds and phosphorylated metabolites are measured using LC-MS MS. Small amounts of NHC-monophosphate (MP) and NHC-diphosphate can be observed, while NHC-triphosphate remains the most abundant metabolite.[1].

NHC-triphosphate triammonium is an active phosphorylated intracellular metabolite of β-d-N4-Hydroxycytidine (NHC) as a triphosphate form[1]. NHC-triphosphate triammonium is a weak alternative substrate for the viral polymerase and can be incorporated into HCV replicon RNA[1][2]. In an intracellular metabolism assay, HCV replicon cells are treated with 10 μM 3H-labeled NHC, and intracellular nucleotide levels are determined after 1, 2 and 8 hours incubations. NHC is rapidly convered into the mono-, di-, and triphosphate forms, and NHC-TP reaches up to 71.12 pM after 8 hours[1].NHC-triphosphate triammonium (NHC-TP) (5-40 μM) absence leads to full-length polymerization products, it can be a weak alternative substrate. In addition, incorporation of NHC-TP instead of CTP increases the molecular weight of the polymerization product by 16 (one extra oxygen) for each event and an obvious electrophoretic shift is observed in cell-free HCV NS5B polymerization reactions[1].Huh-7 cells are incubated with (10-50 μM; 4 h) NHC or a McGuigan phosphoramidate prodrug of NHC. Intracellular levels of the parental compounds and phosphorylated metabolites are measured using LC-MS MS. Small amounts of NHC-monophosphate (MP) and NHC-diphosphate (DP) can be observed, while NHC-triphosphate triammonium remains the most abundant metabolite[2].NHC-triphosphate triammonium (NHC-TP) metabolite may directly target the viral polymerase and behave as a nonobligate chain terminator. It plays a prominent role in inhibiting early negative-strand RNA synthesis, either through chain termination or mutagenesis, which may in turn interfere with correct replicase complex formation. [1]. Stuyver LJ,et al. Ribonucleoside analogue that blocks replication of bovine viral diarrhea and hepatitis C viruses in culture.Antimicrob Agents Chemother. 2003 Jan;47(1):244-54. [2]. Maryam Ehteshami, et al. Characterization of β-d- N4-Hydroxycytidine as a Novel Inhibitor of Chikungunya Virus.

STING agonist C11 is an agonist of the stimulator of interferon genes (STING) pathway.1 It induces secretion of type I IFN from THF and MM6 cells when used at a concentration of 50 μM. STING agonist C11 induces phosphorylation of IFN regulatory factor 3 (IRF3) and increases expression of IFIT1 and viperin, but not IL-1β, IL-6, or IL-8 in THF cells in a STING-dependent manner. It reduces viral titers of chikungunya, Venezuelan equine encephalitis, o'nyong-nyong, Mayaro, and Ross River viruses grown in THF cells (EC90s = 16.44, 16.7, 18.84, 25.19, and 22.57 μM, respectively), an effect that is dependent on the presence of STING and the IFN-α β receptor (IFNAR).References1. Gall, B., Pryke, K., Abraham, J., et al. Emerging alphaviruses are sensitive to cellular states induced by a novel small-molecule agonist of the STING pathway. J. Virol. 92(6), e01913-01917 (2018). STING agonist C11 is an agonist of the stimulator of interferon genes (STING) pathway.1 It induces secretion of type I IFN from THF and MM6 cells when used at a concentration of 50 μM. STING agonist C11 induces phosphorylation of IFN regulatory factor 3 (IRF3) and increases expression of IFIT1 and viperin, but not IL-1β, IL-6, or IL-8 in THF cells in a STING-dependent manner. It reduces viral titers of chikungunya, Venezuelan equine encephalitis, o'nyong-nyong, Mayaro, and Ross River viruses grown in THF cells (EC90s = 16.44, 16.7, 18.84, 25.19, and 22.57 μM, respectively), an effect that is dependent on the presence of STING and the IFN-α β receptor (IFNAR). References1. Gall, B., Pryke, K., Abraham, J., et al. Emerging alphaviruses are sensitive to cellular states induced by a novel small-molecule agonist of the STING pathway. J. Virol. 92(6), e01913-01917 (2018).

Tat-beclin 1, a peptide derived from the autophagy protein beclin 1, is a powerful inducer of autophagy. It interacts with GAPR-1 (GLIPR2), a negative regulator of autophagy. Tat-beclin 1 effectively reduces the buildup of polyglutamine expansion protein aggregates and inhibits the replication of various pathogens, such as HIV-1, in laboratory experiments. In addition, it has demonstrated the ability to decrease mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV).

AKOS B018304 是芳基衍生物，能够在para位置进行极性替换。AKOS B018304 是一种基孔肯雅病毒抑制剂.

Tat-beclin 1 TFA是一种来源于自噬蛋白区域(beclin 1)的肽，有效诱导自噬(autophagy)并与GAPR-1 (GLIPR2)发生相互作用，具有显著的自噬负调控作用。该化合物能有效减少体外聚谷氨酰胺扩增蛋白聚集体的积累，并抑制HIV-1等多种病原体的复制。同时，Tat-beclin 1 TFA能显著降低感染基孔肯雅病(CHIKV)或西尼罗河病毒(WNV)小鼠的死亡率。

L-Sulforaphane 是高效的Keap1 Nrf2 ARE途径诱导剂。与 S-异构体相比，它对大鼠肝脏和肺部的致癌解毒酶系统的诱导能力更强。

CHIKV-IN-4 (compound 31b) acts as a potent and selective inhibitor of the Chikungunya virus, displaying an EC50 value of 0.6 μM [1].

beta-Amyrone (β-Amyron) 对基孔肯雅病毒复制具有抗真菌活性，EC50 为 86 uM。 beta-Amyrone 通过抑制 COX-2 的表达而具有抗炎活性。 beta-Amyrone 表现出抗α-葡萄糖苷酶抑制活性和中等 AChE 活性。 β-Amyrone 可用于炎症、感染和肥胖等疾病的研究。