购物车 
-
加利司韦
- names：
Galidesivir
- CAS号：
249503-25-1
MDL Number： MFCD28385877 - MF(分子式)： C11H15N5O3 MW(分子量)： 265.27
- EINECS: Reaxys Number:
- Pubchem ID:10445549 Brand:BIOFOUNT
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一种腺苷类似物和直接作用的抗病毒药物，能破坏病毒RNA依赖的RNA聚合酶 （RdRp）活性。Galidesivir在体外对多种RNA病毒病原体具有活性，包括丝状病毒和新兴的感染因子，例如MERS-CoV，SARS-CoV和SARS-CoV-2。Galidesivir对某些负义RNA病毒的EC50 在3-68μM。
| 货品编码 | 规格 | 纯度 | 价格 (¥) | 现价(¥) | 特价(¥) | 库存描述 | 数量 | 总计 (¥) |
|---|---|---|---|---|---|---|---|---|
| YZM000436-1mg | 1mg | 99.29% | ¥ 4875.00 | ¥ 4875.00 | 1-3天 | ¥ 0.00 |
| 中文别名 | 加利司韦(249503-25-1);加利地韦;2-（4-氨基-5H-吡咯并（3,2-d）嘧啶-7-基）-5-（羟甲基）吡咯烷-3,4-二醇;BCX-4430;BCX4430;加利地韦;ImmA cpd;免疫素A; |
| 英文别名 | Galidesivir(249503-25-1);BCX-4430 freebase; BCX 4430 freebase; BCX4430 freebase; Immucillin-A; Immucillin A;2-(4-amino-5H-pyrrolo(3,2-d)pyrimidin-7-yl)-5-(hydroxymethyl)pyrrolidine-3,4-diol;BCX-4430;BCX4430;Galidesivir;ImmA cpd;immucillin A;immucillin-A; |
| CAS号 | 249503-25-1 |
| SMILES | O[C@H]1[C@H](C2=CNC3=C2N=CN=C3N)N[C@H](CO)[C@H]1O |
| Inchi | InChI=1S/C11H15N5O3/c12-11-8-6(14-3-15-11)4(1-13-8)7-10(19)9(18)5(2-17)16-7/h1,3,5,7,9-10,13,16-19H,2H2,(H2,12,14,15)/t5-,7+,9-,10+/m1/s1 |
| InchiKey | AMFDITJFBUXZQN-KUBHLMPHSA-N |
| 分子式 Formula | C11H15N5O3 |
| 分子量 Molecular Weight | 265.27 |
| 闪点 FP | 353.7±31.5 °C |
| 熔点 Melting point | No data available |
| 沸点 Boiling point | 661.2±55.0 °C at 760 mmHg |
| Polarizability极化度 | 27.1±0.5 10-24cm3 |
| 密度 Density | 1.6±0.1 g/cm3 |
| 蒸汽压 Vapor Pressure | 0.0±2.1 mmHg at 25°C |
| 溶解度Solubility | 生物体外In Vitro:H2O : 1.53 mg/mL(5.77 mM;Need ultrasonic and warming) |
| 性状 | 固体粉末,Power |
| 储藏条件 Storage conditions | -20°C 3 years年 4°C 2 years年 / In solvent溶液中:-80°C 6 months月 -20°C 1 month月 |
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)作用机理：
Galidesivir通过与天然核苷酸会结合的病毒RNA聚合酶结合而起作用，由于静电相互作用的改变，导致病毒酶的结构变化。病毒RNA聚合酶活性的破坏导致伸长的RNA链过早终止。
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)实验注意事项：
1.实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害
3.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.
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| 产品说明 | 加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一种病毒RNA依赖性RNA聚合酶(RdRp)抑制剂,证明在多种病毒中具有广谱活性 |
| Introduction | 加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A) is a viral RNAependentRNA polymerase inhibitor; |
| Application1 | 加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)demonstrated broadpectrum activity in multiple viruses and a favorable preliminary preclinical safety prof ile. |
| Application2 | 加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一种新型的合成腺苷类似物,可抑制人类细胞中不同丝状病毒的感染,,并具有良好的临床前初步安全性。 |
| Application3 |
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)药理学：
1、BCX4430是一种新型的合成腺苷类似物，可抑制人类细胞中不同丝状病毒的感染。干扰复制过程是一种行之有效的抗病毒策略，已成功地用于开发挽救生命的药物，如HIV核苷抑制剂和阿昔洛韦用于单纯疱疹复合体。BCX4430可能适合通过静脉（IV），肌内（IM）和口服（PO）途径给药。
2、Galidesivir是一种腺苷类似物，已被研究用于对抗Zaire埃博拉病毒。在动物研究中，加利地韦有效提高了由各种病原体（包括埃博拉病毒，马尔堡病毒，黄热病病毒和寨卡病毒）引起的感染的存活率。在体外，它显示出对各种负，正义RNA病毒（包括冠状病毒，丝状病毒和沙粒病毒）的广谱抗病毒活性。1期临床试验已开始确定该药物在人体中的安全性。由于它具有抗其他冠状病毒的活性，因此可以作为COVID-19的潜在疗法进行研究。Galidesivir是一种腺苷类似物，对RNA病毒具有广谱抗病毒活性，其中包括黄病毒，多哥病毒，布尼亚病毒，芳烃病毒，副粘病毒，冠状病毒，丝状病毒，正粘病毒和小核糖核酸病毒。
3、细胞激酶将Galidesivir（BCX4430）磷酸化为模仿ATP的三磷酸；病毒RNA聚合酶将药物的单磷酸核苷酸整合到正在增长的RNA链中，导致链过早终止。Galidesivir有效抑制YFV感染Vero细胞。通过中性红吸收法测定的EC50为8.3μg/ ml（24.5μM）。
4、加利司韦是抗病毒剂，加利司韦用于预防或治疗病毒性疾病的药物。加利司韦可能发挥作用的方式包括通过抑制病毒DNA聚合酶来防止病毒复制。加利司韦与特定的细胞表面受体结合并抑制病毒渗透或脱壳；加利司韦可以抑制病毒蛋白质合成；加利司韦或阻止病毒组装的后期。
5、BCX4430（Immucillin-A）是一种病毒RNA依赖性RNA聚合酶（RdRp）抑制剂；证明在多种病毒中具有广谱活性，并具有良好的临床前初步安全性。IC50值：目标：RdRp抑制剂BCX4430，一种新型的合成腺苷类似物，抑制人细胞中不同丝状病毒的感染。干扰复制过程是一种行之有效的抗病毒策略，已成功地用于开发挽救生命的药物，如HIV核苷抑制剂和阿昔洛韦用于单纯疱疹复合体。BCX4430可能适合通过静脉（IV），肌内（IM）和口服（PO）途径给药。
1、BCX4430是一种新型的合成腺苷类似物，可抑制人类细胞中不同丝状病毒的感染。干扰复制过程是一种行之有效的抗病毒策略，已成功地用于开发挽救生命的药物，如HIV核苷抑制剂和阿昔洛韦用于单纯疱疹复合体。BCX4430可能适合通过静脉（IV），肌内（IM）和口服（PO）途径给药。
2、Galidesivir是一种腺苷类似物，已被研究用于对抗Zaire埃博拉病毒。在动物研究中，加利地韦有效提高了由各种病原体（包括埃博拉病毒，马尔堡病毒，黄热病病毒和寨卡病毒）引起的感染的存活率。在体外，它显示出对各种负，正义RNA病毒（包括冠状病毒，丝状病毒和沙粒病毒）的广谱抗病毒活性。1期临床试验已开始确定该药物在人体中的安全性。由于它具有抗其他冠状病毒的活性，因此可以作为COVID-19的潜在疗法进行研究。Galidesivir是一种腺苷类似物，对RNA病毒具有广谱抗病毒活性，其中包括黄病毒，多哥病毒，布尼亚病毒，芳烃病毒，副粘病毒，冠状病毒，丝状病毒，正粘病毒和小核糖核酸病毒。
3、细胞激酶将Galidesivir（BCX4430）磷酸化为模仿ATP的三磷酸；病毒RNA聚合酶将药物的单磷酸核苷酸整合到正在增长的RNA链中，导致链过早终止。Galidesivir有效抑制YFV感染Vero细胞。通过中性红吸收法测定的EC50为8.3μg/ ml（24.5μM）。
4、加利司韦是抗病毒剂，加利司韦用于预防或治疗病毒性疾病的药物。加利司韦可能发挥作用的方式包括通过抑制病毒DNA聚合酶来防止病毒复制。加利司韦与特定的细胞表面受体结合并抑制病毒渗透或脱壳；加利司韦可以抑制病毒蛋白质合成；加利司韦或阻止病毒组装的后期。
5、BCX4430（Immucillin-A）是一种病毒RNA依赖性RNA聚合酶（RdRp）抑制剂；证明在多种病毒中具有广谱活性，并具有良好的临床前初步安全性。IC50值：目标：RdRp抑制剂BCX4430，一种新型的合成腺苷类似物，抑制人细胞中不同丝状病毒的感染。干扰复制过程是一种行之有效的抗病毒策略，已成功地用于开发挽救生命的药物，如HIV核苷抑制剂和阿昔洛韦用于单纯疱疹复合体。BCX4430可能适合通过静脉（IV），肌内（IM）和口服（PO）途径给药。
| 警示图 | |
| 危险性 | warning |
| 危险性警示 | Not available |
| 安全声明 | H303吞入可能有害+H313皮肤接触可能有害+H2413吸入可能对身体有害 |
| 安全防护 | P264处理后彻底清洗+P280戴防护手套/穿防护服/戴防护眼罩/戴防护面具+P305如果进入眼睛+P351用水小心冲洗几分钟+P338取出隐形眼镜（如果有）并且易于操作,继续冲洗+P337如果眼睛刺激持续+P2393获得医疗建议/护理 |
| 备注 | 实验过程中防止吸入、食入，做好安全防护 |
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)危害标识：
| Taylor R, et al. BCX4430 - A broad-spectrum antiviral adenosine nucleoside analog under development for the treatment of Ebola virus disease. J Infect Public Health. 2016;9(3):220-226. |
| Elfiky AA, et al. ICN-1229, Remdesivir, PSI-7977, Galidesivir, and GS 1278 against SARS-CoV-2 RNA dependent RNA polymerase (RdRp): A molecular docking study. Life Sci. 2020 Mar 25:117592. |
| Warren TK, et al. Protection against filovirus diseases by a novel broad-spectrum nucleoside analogue BCX4430. Nature. 2014;508(7496):402-405. |
| Julander JG, et al. BCX4430, a novel nucleoside analog, effectively treats yellow fever in a Hamster model. Antimicrob Agents Chemother. 2014;58(11):6607-6614. |
| Tchesnokov EP, Feng JY, Porter DP, Gotte M: Mechanism of Inhibition of Ebola Virus RNA-Dependent RNA Polymerase by Remdesivir. Viruses. 2019 Apr 4;11(4). pii: v11040326. doi: 10.3390/v11040326. [PMID: |
加利司韦(249503-25-1,Galidesivir,BCX4430,Immucillin-A)参考文献：
1.Galidesivir limits Rift Valley fever virus infection and disease in Syrian golden hamsters.
Westover JB;Mathis A;Taylor R;Wandersee L;Bailey KW;Sefing EJ;Hickerson BT;Jung KH;Sheridan WP;Gowen BB Antiviral Res. 2018 Aug;156:38-45. doi: 10.1016/j.antiviral.2018.05.013. Epub 2018 Jun 1.
Rift Valley fever virus (RVFV) is a mosquito-borne pathogen endemic to sub-Saharan Africa and the Arabian Peninsula. There are no approved antiviral therapies or vaccines available to treat or prevent severe disease associated with RVFV infection in humans. The adenosine analog, galidesivir (BCX4430), is a broad-spectrum antiviral drug candidate with in vitro antiviral potency (EC;50; of less than 50?μM) in more than 20 different viruses across eight different virus families. Here we report on the activity of galidesivir in the hamster model of peracute RVFV infection. Intramuscular and intraperitoneal treatments effectively limited systemic RVFV (strain ZH501) infection as demonstrated by significantly improved survival outcomes and the absence of infectious virus in the spleen and the majority of the serum, brain, and liver samples collected from infected animals. Our findings support the further development of galidesivir as an antiviral therapy for use in treating severe RVFV infection, and possibly other related phleboviral diseases.
2、Mechanism of Inhibition of Ebola Virus RNA-Dependent RNA Polymerase by Remdesivir
Egor P Tchesnokov 1 2, Joy Y Feng 3, Danielle P Porter 4, Matthias Götte
Abstract Remdesivir (GS-5734) is a 1'-cyano-substituted adenosine nucleotide analogue prodrug that shows broad-spectrum antiviral activity against several RNA viruses. This compound is currently under clinical development for the treatment of Ebola virus disease (EVD). While antiviral effects have been demonstrated in cell culture and in non-human primates, the mechanism of action of Ebola virus (EBOV) inhibition for remdesivir remains to be fully elucidated. The EBOV RNA-dependent RNA polymerase (RdRp) complex was recently expressed and purified, enabling biochemical studies with the relevant triphosphate (TP) form of remdesivir and its presumptive target. In this study, we confirmed that remdesivir-TP is able to compete for incorporation with adenosine triphosphate (ATP). Enzyme kinetics revealed that EBOV RdRp and respiratory syncytial virus (RSV) RdRp incorporate ATP and remdesivir-TP with similar efficiencies. The selectivity of ATP against remdesivir-TP is ~4 for EBOV RdRp and ~3 for RSV RdRp. In contrast, purified human mitochondrial RNA polymerase (h-mtRNAP) effectively discriminates against remdesivir-TP with a selectivity value of ~500-fold. For EBOV RdRp, the incorporated inhibitor at position i does not affect the ensuing nucleotide incorporation event at position i+1. For RSV RdRp, we measured a ~6-fold inhibition at position i+1 although RNA synthesis was not terminated. Chain termination was in both cases delayed and was seen predominantly at position i+5. This pattern is specific to remdesivir-TP and its 1'-cyano modification. Compounds with modifications at the 2'-position show different patterns of inhibition. While 2'-C-methyl-ATP is not incorporated, ara-ATP acts as a non-obligate chain terminator and prevents nucleotide incorporation at position i+1. Taken together, our biochemical data indicate that the major contribution to EBOV RNA synthesis inhibition by remdesivir can be ascribed to delayed chain termination. The long distance of five residues between the incorporated nucleotide analogue and its inhibitory effect warrant further investigation.
3、Galidesivir limits Rift Valley fever virus infection and disease in Syrian golden hamsters
Jonna B Westover 1, Amanda Mathis 2, Ray Taylor 2, Luci Wandersee 1, Kevin W Bailey 1, Eric J Sefing 1, Brady T Hickerson 1, Kie-Hoon Jung 1, William P Sheridan 2, Brian B Gowen
Abstract Rift Valley fever virus (RVFV) is a mosquito-borne pathogen endemic to sub-Saharan Africa and the Arabian Peninsula. There are no approved antiviral therapies or vaccines available to treat or prevent severe disease associated with RVFV infection in humans. The adenosine analog, galidesivir (BCX4430), is a broad-spectrum antiviral drug candidate with in vitro antiviral potency (EC50 of less than 50 μM) in more than 20 different viruses across eight different virus families. Here we report on the activity of galidesivir in the hamster model of peracute RVFV infection. Intramuscular and intraperitoneal treatments effectively limited systemic RVFV (strain ZH501) infection as demonstrated by significantly improved survival outcomes and the absence of infectious virus in the spleen and the majority of the serum, brain, and liver samples collected from infected animals. Our findings support the further development of galidesivir as an antiviral therapy for use in treating severe RVFV infection, and possibly other related phleboviral diseases.
4、Protection against filovirus diseases by a novel broad-spectrum nucleoside analogue BCX4430
Travis K Warren 1, Jay Wells 1, Rekha G Panchal 1, Kelly S Stuthman 1, Nicole L Garza 1, Sean A Van Tongeren 1, Lian Dong 1, Cary J Retterer 1, Brett P Eaton 1, Gianluca Pegoraro 1, Shelley Honnold 1, Shanta Bantia 2, Pravin Kotian 2, Xilin Chen 2, Brian R Taubenheim 3, Lisa S Welch 1, Dena M Minning 4, Yarlagadda S Babu 2, William P Sheridan 2, Sina Bavari
Abstract Filoviruses are emerging pathogens and causative agents of viral haemorrhagic fever. Case fatality rates of filovirus disease outbreaks are among the highest reported for any human pathogen, exceeding 90% (ref. 1). Licensed therapeutic or vaccine products are not available to treat filovirus diseases. Candidate therapeutics previously shown to be efficacious in non-human primate disease models are based on virus-specific designs and have limited broad-spectrum antiviral potential. Here we show that BCX4430, a novel synthetic adenosine analogue, inhibits infection of distinct filoviruses in human cells. Biochemical, reporter-based and primer-extension assays indicate that BCX4430 inhibits viral RNA polymerase function, acting as a non-obligate RNA chain terminator. Post-exposure intramuscular administration of BCX4430 protects against Ebola virus and Marburg virus disease in rodent models. Most importantly, BCX4430 completely protects cynomolgus macaques from Marburg virus infection when administered as late as 48 hours after infection. In addition, BCX4430 exhibits broad-spectrum antiviral activity against numerous viruses, including bunyaviruses, arenaviruses, paramyxoviruses, coronaviruses and flaviviruses. This is the first report, to our knowledge, of non-human primate protection from filovirus disease by a synthetic drug-like small molecule. We provide additional pharmacological characterizations supporting the potential development of BCX4430 as a countermeasure against human filovirus diseases and other viral diseases representing major public health threats.
1.Galidesivir limits Rift Valley fever virus infection and disease in Syrian golden hamsters.
Westover JB;Mathis A;Taylor R;Wandersee L;Bailey KW;Sefing EJ;Hickerson BT;Jung KH;Sheridan WP;Gowen BB Antiviral Res. 2018 Aug;156:38-45. doi: 10.1016/j.antiviral.2018.05.013. Epub 2018 Jun 1.
Rift Valley fever virus (RVFV) is a mosquito-borne pathogen endemic to sub-Saharan Africa and the Arabian Peninsula. There are no approved antiviral therapies or vaccines available to treat or prevent severe disease associated with RVFV infection in humans. The adenosine analog, galidesivir (BCX4430), is a broad-spectrum antiviral drug candidate with in vitro antiviral potency (EC;50; of less than 50?μM) in more than 20 different viruses across eight different virus families. Here we report on the activity of galidesivir in the hamster model of peracute RVFV infection. Intramuscular and intraperitoneal treatments effectively limited systemic RVFV (strain ZH501) infection as demonstrated by significantly improved survival outcomes and the absence of infectious virus in the spleen and the majority of the serum, brain, and liver samples collected from infected animals. Our findings support the further development of galidesivir as an antiviral therapy for use in treating severe RVFV infection, and possibly other related phleboviral diseases.
2、Mechanism of Inhibition of Ebola Virus RNA-Dependent RNA Polymerase by Remdesivir
Egor P Tchesnokov 1 2, Joy Y Feng 3, Danielle P Porter 4, Matthias Götte
Abstract Remdesivir (GS-5734) is a 1'-cyano-substituted adenosine nucleotide analogue prodrug that shows broad-spectrum antiviral activity against several RNA viruses. This compound is currently under clinical development for the treatment of Ebola virus disease (EVD). While antiviral effects have been demonstrated in cell culture and in non-human primates, the mechanism of action of Ebola virus (EBOV) inhibition for remdesivir remains to be fully elucidated. The EBOV RNA-dependent RNA polymerase (RdRp) complex was recently expressed and purified, enabling biochemical studies with the relevant triphosphate (TP) form of remdesivir and its presumptive target. In this study, we confirmed that remdesivir-TP is able to compete for incorporation with adenosine triphosphate (ATP). Enzyme kinetics revealed that EBOV RdRp and respiratory syncytial virus (RSV) RdRp incorporate ATP and remdesivir-TP with similar efficiencies. The selectivity of ATP against remdesivir-TP is ~4 for EBOV RdRp and ~3 for RSV RdRp. In contrast, purified human mitochondrial RNA polymerase (h-mtRNAP) effectively discriminates against remdesivir-TP with a selectivity value of ~500-fold. For EBOV RdRp, the incorporated inhibitor at position i does not affect the ensuing nucleotide incorporation event at position i+1. For RSV RdRp, we measured a ~6-fold inhibition at position i+1 although RNA synthesis was not terminated. Chain termination was in both cases delayed and was seen predominantly at position i+5. This pattern is specific to remdesivir-TP and its 1'-cyano modification. Compounds with modifications at the 2'-position show different patterns of inhibition. While 2'-C-methyl-ATP is not incorporated, ara-ATP acts as a non-obligate chain terminator and prevents nucleotide incorporation at position i+1. Taken together, our biochemical data indicate that the major contribution to EBOV RNA synthesis inhibition by remdesivir can be ascribed to delayed chain termination. The long distance of five residues between the incorporated nucleotide analogue and its inhibitory effect warrant further investigation.
3、Galidesivir limits Rift Valley fever virus infection and disease in Syrian golden hamsters
Jonna B Westover 1, Amanda Mathis 2, Ray Taylor 2, Luci Wandersee 1, Kevin W Bailey 1, Eric J Sefing 1, Brady T Hickerson 1, Kie-Hoon Jung 1, William P Sheridan 2, Brian B Gowen
Abstract Rift Valley fever virus (RVFV) is a mosquito-borne pathogen endemic to sub-Saharan Africa and the Arabian Peninsula. There are no approved antiviral therapies or vaccines available to treat or prevent severe disease associated with RVFV infection in humans. The adenosine analog, galidesivir (BCX4430), is a broad-spectrum antiviral drug candidate with in vitro antiviral potency (EC50 of less than 50 μM) in more than 20 different viruses across eight different virus families. Here we report on the activity of galidesivir in the hamster model of peracute RVFV infection. Intramuscular and intraperitoneal treatments effectively limited systemic RVFV (strain ZH501) infection as demonstrated by significantly improved survival outcomes and the absence of infectious virus in the spleen and the majority of the serum, brain, and liver samples collected from infected animals. Our findings support the further development of galidesivir as an antiviral therapy for use in treating severe RVFV infection, and possibly other related phleboviral diseases.
4、Protection against filovirus diseases by a novel broad-spectrum nucleoside analogue BCX4430
Travis K Warren 1, Jay Wells 1, Rekha G Panchal 1, Kelly S Stuthman 1, Nicole L Garza 1, Sean A Van Tongeren 1, Lian Dong 1, Cary J Retterer 1, Brett P Eaton 1, Gianluca Pegoraro 1, Shelley Honnold 1, Shanta Bantia 2, Pravin Kotian 2, Xilin Chen 2, Brian R Taubenheim 3, Lisa S Welch 1, Dena M Minning 4, Yarlagadda S Babu 2, William P Sheridan 2, Sina Bavari
Abstract Filoviruses are emerging pathogens and causative agents of viral haemorrhagic fever. Case fatality rates of filovirus disease outbreaks are among the highest reported for any human pathogen, exceeding 90% (ref. 1). Licensed therapeutic or vaccine products are not available to treat filovirus diseases. Candidate therapeutics previously shown to be efficacious in non-human primate disease models are based on virus-specific designs and have limited broad-spectrum antiviral potential. Here we show that BCX4430, a novel synthetic adenosine analogue, inhibits infection of distinct filoviruses in human cells. Biochemical, reporter-based and primer-extension assays indicate that BCX4430 inhibits viral RNA polymerase function, acting as a non-obligate RNA chain terminator. Post-exposure intramuscular administration of BCX4430 protects against Ebola virus and Marburg virus disease in rodent models. Most importantly, BCX4430 completely protects cynomolgus macaques from Marburg virus infection when administered as late as 48 hours after infection. In addition, BCX4430 exhibits broad-spectrum antiviral activity against numerous viruses, including bunyaviruses, arenaviruses, paramyxoviruses, coronaviruses and flaviviruses. This is the first report, to our knowledge, of non-human primate protection from filovirus disease by a synthetic drug-like small molecule. We provide additional pharmacological characterizations supporting the potential development of BCX4430 as a countermeasure against human filovirus diseases and other viral diseases representing major public health threats.
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