3d7 p. falciparum

SARS-CoV-IN-1 is an effective SARS-CoV replication inhibitor(EC50 of 4.9 μM in Vero cells).

SARS-CoV-IN-2 is an effective SARS-CoV replication inhibitor

SARS-CoV-IN-3 is an effective SARS-CoV replication inhibitor.

Didesethyl chloroquine (Bisdesethylchloroquine) 是一种有效的心肌抑制剂。Didesethyl chloroquine 是抗疟药氯喹的主要代谢产物。

CWHM-1008 is an effective oral antimalarial drug. The EC50 values of the drug-sensitive Plasmodium falciparum 3D7 and drug-resistant Dd2 strains are 46 and 21 nM, respectively.

LysRs-IN-2 是一种赖氨酸 tRNA 合成酶 (KRS) 抑制剂，有抗寄生虫感染的作用，抑制恶性疟原虫 KRS (PfKRS) 和小隐孢子虫 KRS (CpKRS) ，可用于研究疟疾感染。

DSM265 (PfSPZ) 是一种具有抗疟活性的二氢乳清酸脱氢酶抑制剂（IC50：8.9 nM）。DSM265 抑制 Pf3D7 寄生虫的生长可用于治疗和预防疟疾感染。

WJM280, 作为一种口服活性抗疟疾化合物，对P. falciparum 3D7寄生虫展示出极高的效力，其EC50值达到了0.04 μM。

SPB07935在恶性疟原虫Plasmodium falciparum中抑制plasmepsin II，具有抗疟功能。该化合物可调节P. falciparum的生命周期，抑制疟原虫不同亚型（FcB1 和 3D7）的生长，IC50分别为8 μM和4.7 μM。

HDAC-IN-88 (Compound HJ-9) 是一种HDAC抑制剂，能够抑制HDAC6、HDAC1、HDAC2、HDAC8和HDAC3，其IC50分别为0.226、1.103、2.308、3.255和3.864 μM。HDAC-IN-88 抑制癌细胞 HepG2、HCT116 和 MV4-11 的增殖，IC50依次为5.47、9.78 和 0.38 μM，并抑制HCT116的迁移，同时在G0 G1期阻滞细胞周期，在MV4-11中引发细胞凋亡 (apoptosis) 和自噬 (autophagy)。HDAC-IN-88 可降低ROS水平和线粒体膜电位，显示出抗疟活性，能够抑制恶性疟原虫P. falciparum3D7，EC50为165 nM。此外，HDAC-IN-88 具备抗血管生成活性。

CCOE-5 是一种查耳酮类化合物，表现出抗疟原虫活性。其对 P. falciparum (3D7) 的 IC50 为 1.4 μg mL，对 P. falciparum (INDO) 的 IC50 小于 5 μg mL。CCOE-5 有望在抗感染研究中发挥作用。

DSM1465 (Compound 82) 是高效选择性的P. falciparum二氢酸脱氢酶 (PfDHODH) 抑制剂，IC50为15 nM，可以抑制P. falciparum3D7 (Pf3D7) 寄生虫，EC50为1.4 nM。在人源化P. falciparum小鼠模型中，DSM1465 展现出强大的体内活性。

Dehydrocorydaline nitrate 是生物碱。Dehydrocorydaline 调节 Bax，Bcl-2蛋白表达，激活 caspase-7，caspase-8，并使 PARP 失活。它能增强 p38 MAPK 活化，具有抗炎、抗癌、抗疟疾等功效。

AN3661, a potent antimalarial lead compound, targets a Plasmodium falciparum cleavage and polyadenylation specificity factor homologue subunit 3 (PfCPSF3). AN3661 inhibits Plasmodium falciparum laboratory-adapted strains, Ugandan field isolates, and murine P. berghei and P. falciparum infections[1]. AN3661 is active at nanomolar (IC50=20-56 nM) concentrations against P. falciparum laboratory strains known to be sensitive (3D7) or resistant (W2, Dd2, K1, HB3, FCR3 and TM90C2B), and AN3661 is similarly active in ex vivo studies of fresh Ugandan field isolates (mean ex vivo IC50=64 nM). AN3661 shows minimal cytotoxicity against mammalian cell lines, with the CC50 60.5 μM against Jurkat cells, and all other CC50 values greater than the highest concentrations tested (25 μM or above)[1].AN3661 inhibits the stability of P. falciparum transcripts[1]. AN3661 (50-200 mg.kg; p.o.; daily for 4 days) inhibits murine P. berghei infections with ED90 (4 days) 0.34 mg kg[1].AN3661 is administered orally for 4 days, beginning on the third day of infection, the ED90 4 days after initiation of treatment is 0.57 mg kg[1]. Animal Model: P. berghei-infected mice (malaria model)[1] [1]. Sonoiki E, et al. A potent antimalarial benzoxaborole targets a Plasmodium falciparum cleavage and polyadenylation specificity factor homologue. Nat Commun. 2017;8:14574. Published 2017 Mar 6.

Purfalcamine is an orally active, selective Plasmodium falciparum calcium-dependent protein kinase 1 (PfCDPK1) inhibitor with an IC50 of 17 nM and an EC50 of 230 nM. Purfalcamine has antimalarial activity and causes malaria parasites developmental arrest at the schizont stage[1][2]. Purfalcamine has low activity against Toxoplasma gondii calcium-dependent protein kinase 3 (TgCDPK3)[1]. Purfalcamine (225, 450 nM) has no effect on the parasitemia in the first 32 hours. After about 40 hours, parasite level remains stable and then begins dropping[1]. Purfalcamine inhibits proliferation with EC50s of 171-259 nM for P. falciparum strains (3D7, Dd2, FCB, HB3 and W2), which indicates effectiveness against drug-resistant parasites[1]. Given that the EC50 value for P. falciparum (3D7) is 230 nM, Purfalcamine shows a therapeutic window ranging from 23-fold to 36-fold (EC50s for CHO=12.33 μM, HEp2=7.235 μM, HeLa=7.029 μM and Huh7=5.476 μM)[1]. Purfalcamine (10 mg kg; oral gavage; BID; for 6 days) demonstrates a delay in the onset of parasitemia in treated mice[1]. Purfalcamine (20 mg kg; orally gavage) exhibits a Cmax of 2.6 μM with a half-life of 3.1 hours[1]. Animal Model: Male BALB c mice, 7 weeks of age with the malaria parasite[1] [1]. Nobutaka Kato, et al. Gene expression signatures and small-molecule compounds link a protein kinase to Plasmodium falciparum motility. Nat Chem Biol. 2008 Jun;4(6):347-56. [2]. Rajshekhar Y Gaji, et al. Expression of the essential Kinase PfCDPK1 from Plasmodium falciparum in Toxoplasma gondii facilitates the discovery of novel antimalarial drugs. Antimicrob Agents Chemother. 2014 May;58(5):2598-607.

JMI-346 可用作抗疟疾剂，可抑制恶性疟原虫菌株的 CQS (3D7) 和 CQR (RKL-9) 菌株生长，IC50 值分别为 13 μM 和 33 μM。JMI-346 是恶性疟原虫 -2 蛋白酶(PfFP-2)的有效抑制剂。

JMI-105 具有用作抗疟剂的潜力。JMI-105 是恶性疟原虫 -2 蛋白酶(PfFP-2)的有效抑制剂，可抑制恶性疟原虫菌株的CQS 株 (3D7) 和 CQR 株 (RKL-9) 的生长，IC50值分别为8.8 μM 和14.3 μM。在伯氏疟原虫 ANKA 感染小鼠模型中，JMI-105 显著降低寄生虫血症并延长宿主存活期。

Phosphodiesterase-IN-1 (Compound 7) 为一种针对磷酸二酯酶（PDE）的抑制剂，表现出对疟原虫的活性。该化合物在抑制P. falciparum（strain 3D7）的增殖方面表现有效，其IC50为0.64 μM。

Fosmidomycin 是一种口服有效的抗生素，通过抑制 1-脱氧-D-木酮糖 5-磷酸 (DOXP) 还原异构酶来展现其抗疟效果。它对恶性疟原虫 P. falciparum 株系 3D7、HB3、Dd2 和 A2 具有抑制作用，其 IC50 值分别为 150、71、170 和 150 ng mL。此外，Fosmidomycin 与 Clindamycin 结合使用时展现协同作用，可增强小鼠体内对疟疾的疗效。

INE963 是快速有效的血液阶段抗疟剂，EC50为 3-6 nM。INE963 有单纯性疟疾的研究潜力。

Melicopine 是一种存在于Z. simulans中的生物碱，具有抗疟疾和抗癌特性。它对氯喹敏感的3D7和对氯喹耐药的Dd2期P. falciparum表现出抑制作用，IC50分别为29.7和33.7 µg mL。对于前列腺癌细胞PC-3M和LNCaP，Melicopine表现出细胞毒性，IC50分别为47.9和37.8 µg mL，但对非癌性HEK293细胞无效 (IC50大于100 µg mL)。Melicopine有潜力用于抗癌和抗感染研究。