購物車 
-
加利司韋
- names：
Galidesivir
- CAS號：
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
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一種腺苷類似物和直接作用的抗病毒藥物，能破壞病毒RNA依賴的RNA聚合酶 （RdRp）活性。Galidesivir在體外對多種RNA病毒病原體具有活性，包括絲狀病毒和新興的感染因子，例如MERS-CoV，SARS-CoV和SARS-CoV-2。Galidesivir對某些負義RNA病毒的EC50 在3-68μM。
| 貨品編碼 | 規格 | 純度 | 價格 (￥) | 現價(￥) | 特價(￥) | 庫存描述 | 數量 | 總計 (￥) |
|---|---|---|---|---|---|---|---|---|
| YZM000436-1mg | 1mg | 99.29% | ￥ 4875.00 | ￥ 4875.00 | 1-3天 | ￥ 0.00 |
| 中文別名 | 加利司韋(249503-25-1);加利地韋;2-（4-氨基-5H-吡咯并（3,2-d）嘧啶-7-基）-5-（羥甲基）吡咯烷-3,4-二醇;BCX-4430;BCX4430;加利地韋;ImmA cpd;免疫素A; |
| 英文別名 | 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號 | 249503-25-1 |
| 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 |
| 溶解度Solubility | 生物體外In Vitro:H2O : 1.53 mg/mL(5.77 mM;Need ultrasonic and warming) |
| 性狀 | 固體粉末,Power |
| 儲藏條件 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 |
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)作用機理：
Galidesivir通過與天然核苷酸會結合的病毒RNA聚合酶結合而起作用，由于靜電相互作用的改變，導致病毒酶的結構變化。病毒RNA聚合酶活性的破壞導致伸長的RNA鏈過早終止。
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)實驗注意事項：
1.實驗前需戴好防護眼鏡，穿戴防護服和口罩，佩戴手套，避免與皮膚接觸。
2.實驗過程中如遇到有毒或者刺激性物質及有害物質產生，必要時實驗操作需要手套箱內完成以免對實驗人員造成傷害
3.實驗后產生的廢棄物需分類存儲，并交于專業生物廢氣物處理公司處理，以免造成環境污染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.
Tags:加利司韋試劑,加利司韋雜質,加利司韋中間體,加利司韋合成,加利司韋密度,加利司韋溶解度,加利司韋旋光度,加利司韋閃點,加利司韋熔點,加利司韋購買,
| 產品說明 | 加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一種病毒RNA依賴性RNA聚合酶(RdRp)抑制劑,證明在多種病毒中具有廣譜活性 |
| Introduction | 加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A) is a viral RNAependentRNA polymerase inhibitor; |
| Application1 | 加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)demonstrated broadpectrum activity in multiple viruses and a favorable preliminary preclinical safety prof ile. |
| Application2 | 加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)是一種新型的合成腺苷類似物,可抑制人類細胞中不同絲狀病毒的感染,,并具有良好的臨床前初步安全性。 |
| Application3 |
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)藥理學：
1、BCX4430是一種新型的合成腺苷類似物，可抑制人類細胞中不同絲狀病毒的感染。干擾復制過程是一種行之有效的抗病毒策略，已成功地用于開發挽救生命的藥物，如HIV核苷抑制劑和阿昔洛韋用于單純皰疹復合體。BCX4430可能適合通過靜脈（IV），肌內（IM）和口服（PO）途徑給藥。
2、Galidesivir是一種腺苷類似物，已被研究用于對抗Zaire埃博拉病毒。在動物研究中，加利地韋有效提高了由各種病原體（包括埃博拉病毒，馬爾堡病毒，黃熱病病毒和寨卡病毒）引起的感染的存活率。在體外，它顯示出對各種負，正義RNA病毒（包括冠狀病毒，絲狀病毒和沙粒病毒）的廣譜抗病毒活性。1期臨床試驗已開始確定該藥物在人體中的安全性。由于它具有抗其他冠狀病毒的活性，因此可以作為COVID-19的潛在療法進行研究。Galidesivir是一種腺苷類似物，對RNA病毒具有廣譜抗病毒活性，其中包括黃病毒，多哥病毒，布尼亞病毒，芳烴病毒，副粘病毒，冠狀病毒，絲狀病毒，正粘病毒和小核糖核酸病毒。
3、細胞激酶將Galidesivir（BCX4430）磷酸化為模仿ATP的三磷酸；病毒RNA聚合酶將藥物的單磷酸核苷酸整合到正在增長的RNA鏈中，導致鏈過早終止。Galidesivir有效抑制YFV感染Vero細胞。通過中性紅吸收法測定的EC50為8.3μg/ ml（24.5μM）。
4、加利司韋是抗病毒劑，加利司韋用于預防或治療病毒性疾病的藥物。加利司韋可能發揮作用的方式包括通過抑制病毒DNA聚合酶來防止病毒復制。加利司韋與特定的細胞表面受體結合并抑制病毒滲透或脫殼；加利司韋可以抑制病毒蛋白質合成；加利司韋或阻止病毒組裝的后期。
5、BCX4430（Immucillin-A）是一種病毒RNA依賴性RNA聚合酶（RdRp）抑制劑；證明在多種病毒中具有廣譜活性，并具有良好的臨床前初步安全性。IC50值：目標：RdRp抑制劑BCX4430，一種新型的合成腺苷類似物，抑制人細胞中不同絲狀病毒的感染。干擾復制過程是一種行之有效的抗病毒策略，已成功地用于開發挽救生命的藥物，如HIV核苷抑制劑和阿昔洛韋用于單純皰疹復合體。BCX4430可能適合通過靜脈（IV），肌內（IM）和口服（PO）途徑給藥。
1、BCX4430是一種新型的合成腺苷類似物，可抑制人類細胞中不同絲狀病毒的感染。干擾復制過程是一種行之有效的抗病毒策略，已成功地用于開發挽救生命的藥物，如HIV核苷抑制劑和阿昔洛韋用于單純皰疹復合體。BCX4430可能適合通過靜脈（IV），肌內（IM）和口服（PO）途徑給藥。
2、Galidesivir是一種腺苷類似物，已被研究用于對抗Zaire埃博拉病毒。在動物研究中，加利地韋有效提高了由各種病原體（包括埃博拉病毒，馬爾堡病毒，黃熱病病毒和寨卡病毒）引起的感染的存活率。在體外，它顯示出對各種負，正義RNA病毒（包括冠狀病毒，絲狀病毒和沙粒病毒）的廣譜抗病毒活性。1期臨床試驗已開始確定該藥物在人體中的安全性。由于它具有抗其他冠狀病毒的活性，因此可以作為COVID-19的潛在療法進行研究。Galidesivir是一種腺苷類似物，對RNA病毒具有廣譜抗病毒活性，其中包括黃病毒，多哥病毒，布尼亞病毒，芳烴病毒，副粘病毒，冠狀病毒，絲狀病毒，正粘病毒和小核糖核酸病毒。
3、細胞激酶將Galidesivir（BCX4430）磷酸化為模仿ATP的三磷酸；病毒RNA聚合酶將藥物的單磷酸核苷酸整合到正在增長的RNA鏈中，導致鏈過早終止。Galidesivir有效抑制YFV感染Vero細胞。通過中性紅吸收法測定的EC50為8.3μg/ ml（24.5μM）。
4、加利司韋是抗病毒劑，加利司韋用于預防或治療病毒性疾病的藥物。加利司韋可能發揮作用的方式包括通過抑制病毒DNA聚合酶來防止病毒復制。加利司韋與特定的細胞表面受體結合并抑制病毒滲透或脫殼；加利司韋可以抑制病毒蛋白質合成；加利司韋或阻止病毒組裝的后期。
5、BCX4430（Immucillin-A）是一種病毒RNA依賴性RNA聚合酶（RdRp）抑制劑；證明在多種病毒中具有廣譜活性，并具有良好的臨床前初步安全性。IC50值：目標：RdRp抑制劑BCX4430，一種新型的合成腺苷類似物，抑制人細胞中不同絲狀病毒的感染。干擾復制過程是一種行之有效的抗病毒策略，已成功地用于開發挽救生命的藥物，如HIV核苷抑制劑和阿昔洛韋用于單純皰疹復合體。BCX4430可能適合通過靜脈（IV），肌內（IM）和口服（PO）途徑給藥。
| 警示圖 | |
| 危險性 | warning |
| 危險性警示 | Not available |
| 安全聲明 | H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對身體有害 |
| 安全防護 | P264處理后徹底清洗+P280戴防護手套/穿防護服/戴防護眼罩/戴防護面具+P305如果進入眼睛+P351用水小心沖洗幾分鐘+P338取出隱形眼鏡（如果有）并且易于操作,繼續沖洗+P337如果眼睛刺激持續+P2393獲得醫療建議/護理 |
| 備注 | 實驗過程中防止吸入、食入，做好安全防護 |
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)危害標識：
| 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: |
加利司韋(249503-25-1,Galidesivir,BCX4430,Immucillin-A)參考文獻：
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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