SrasV1, Main, Curation, bibRecord, 003491

Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model

Identifieur interne : 003491 ( Main/Curation ); précédent : 003490; suivant : 003492

Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model

Auteurs : Dale L. Barnard [États-Unis] ; Craig W. Day [États-Unis] ; Kevin Bailey [États-Unis] ; Matthew Heiner [États-Unis] ; Robert Montgomery [États-Unis] ; Larry Lauridsen [États-Unis] ; Kie-Hoon Jung [États-Unis] ; Joseph K.-K. Li [États-Unis] ; Paul K. S. Chan [Hong Kong] ; Robert W. Sidwell [États-Unis]

Source :

Antiviral research [ 0166-3542 ] ; 2008.

RBID : Pascal:08-0298379

Descripteurs français

KwdFr :
- Animaux, Antiviraux (administration et posologie), Antiviraux (pharmacologie), Antiviraux (toxicité), Antiviraux (usage thérapeutique), Cellules Vero, Chimioprévention, Cytokines (analyse), Femelle, Phénothiazines (administration et posologie), Phénothiazines (pharmacologie), Phénothiazines (toxicité), Phénothiazines (usage thérapeutique), Poumon (anatomopathologie), Poumon (virologie), Rouge neutre (métabolisme), Réplication virale, Souris, Souris de lignée BALB C, Structure moléculaire, Survie cellulaire, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (traitement médicamenteux), Virus du SRAS ().
MESH :
- administration et posologie : Antiviraux, Phénothiazines.
- analyse : Cytokines.
- anatomopathologie : Poumon.
- métabolisme : Rouge neutre.
- pharmacologie : Antiviraux, Phénothiazines.
- toxicité : Antiviraux, Phénothiazines.
- traitement médicamenteux : Syndrome respiratoire aigu sévère.
- usage thérapeutique : Antiviraux, Phénothiazines.
- virologie : Poumon.
Pascal (Inist)
- Animaux, Antipsychotique, Cellules Vero, Chimioprévention, Femelle, Neuroleptique, Relation structure activité, Promazine, Antiviral, Réplication virale, Souris, Souris de lignée BALB C, Structure moléculaire, Survie cellulaire, Syndrome respiratoire aigu sévère, Virus du SRAS, Virus syndrome respiratoire aigu sévère, Réplication, Modèle animal, Souris, Psychotrope.

English descriptors

KwdEn :
- Animal model, Animals, Antipsychotic, Antiviral, Antiviral Agents (administration & dosage), Antiviral Agents (pharmacology), Antiviral Agents (therapeutic use), Antiviral Agents (toxicity), Cell Survival, Chemoprevention, Chlorocebus aethiops, Cytokines (analysis), Female, Lung (pathology), Lung (virology), Mice, Mice, Inbred BALB C, Molecular Structure, Mouse, Neuroleptic, Neutral Red (metabolism), Phenothiazines (administration & dosage), Phenothiazines (pharmacology), Phenothiazines (therapeutic use), Phenothiazines (toxicity), Promazine, Psychotropic, Replication, SARS Virus (drug effects), Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (prevention & control), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Structure activity relation, Vero Cells, Virus Replication.
MESH :
- chemical , administration & dosage : Antiviral Agents, Phenothiazines.
- chemical , analysis : Cytokines.
- chemical , metabolism : Neutral Red.
- chemical , pharmacology : Antiviral Agents, Phenothiazines.
- chemical , therapeutic use : Antiviral Agents, Phenothiazines.
- chemical , toxicity : Antiviral Agents, Phenothiazines.
- drug effects : SARS Virus.
- drug therapy : Severe Acute Respiratory Syndrome.
- pathology : Lung.
- prevention & control : Severe Acute Respiratory Syndrome.
- virology : Lung.
- Animals, Cell Survival, Chemoprevention, Chlorocebus aethiops, Female, Mice, Mice, Inbred BALB C, Molecular Structure, Vero Cells, Virus Replication.

Abstract

Phenothiazine and derivatives were tested for inhibition of SARS-CoV replication. Phenothiazine slightly inhibited SARS-CoV replication in a neutral red (NR) uptake assay. Adding a propylamino group to give promazine reduced virus yields (VYR assay) with an EC₉₀ = 8.3 ± 2.8 μM, but without selectivity. Various substitutions in the basic phenothiazine structure did not promote efficacy. Phenazine ethosulfate was the most potent compound by VYR assay (EC₉₀ = 6.1 ± 4.3 μM). All compounds were toxic (IC₅₀ = 6.6-74.5 μM) except for phenoxathiin (IC₅₀ = 858 ± 208 μM) and 10-(alpha-diethylamino-propionyl) phenothiazine.HCl (IC₅₀ =195 ± 71.2 μM). Consequently, none were selective inhibitors of SARS-CoV replication (SI values <1-3.3 μM). These data portended the poor efficacy of promazine in a SARS-CoV mouse lung replication model. Intraperitoneal treatment with promazine using a prophylactic (-4 h)/therapeutic regimen of 1, 10, or 50 mg/(kg day) did not reduce virus lung titers at day 3, yet prolonged virus replication to 14 days. Similar therapeutic promazine doses were not efficacious. Thus, promazine did not affect SARS-CoV replication in vitro or in vivo, nor were any other phenothiazines efficacious in reducing virus replication. Therefore, treating SARS infections with compounds like promazine is not warranted.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2582943

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Le document en format XML

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<term>Animals</term>
<term>Antipsychotic</term>
<term>Antiviral</term>
<term>Antiviral Agents (administration & dosage)</term>
<term>Antiviral Agents (pharmacology)</term>
<term>Antiviral Agents (therapeutic use)</term>
<term>Antiviral Agents (toxicity)</term>
<term>Cell Survival</term>
<term>Chemoprevention</term>
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<term>Cytokines (analysis)</term>
<term>Female</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Molecular Structure</term>
<term>Mouse</term>
<term>Neuroleptic</term>
<term>Neutral Red (metabolism)</term>
<term>Phenothiazines (administration & dosage)</term>
<term>Phenothiazines (pharmacology)</term>
<term>Phenothiazines (therapeutic use)</term>
<term>Phenothiazines (toxicity)</term>
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<term>Severe Acute Respiratory Syndrome (prevention & control)</term>
<term>Severe acute respiratory syndrome</term>
<term>Severe acute respiratory syndrome virus</term>
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<front><div type="abstract" xml:lang="en">Phenothiazine and derivatives were tested for inhibition of SARS-CoV replication. Phenothiazine slightly inhibited SARS-CoV replication in a neutral red (NR) uptake assay. Adding a propylamino group to give promazine reduced virus yields (VYR assay) with an EC<sub>90</sub>
 = 8.3 ± 2.8 μM, but without selectivity. Various substitutions in the basic phenothiazine structure did not promote efficacy. Phenazine ethosulfate was the most potent compound by VYR assay (EC<sub>90</sub>
 = 6.1 ± 4.3 μM). All compounds were toxic (IC<sub>50</sub>
 = 6.6-74.5 μM) except for phenoxathiin (IC<sub>50</sub>
 = 858 ± 208 μM) and 10-(alpha-diethylamino-propionyl) phenothiazine.HCl (IC<sub>50</sub>
 =195 ± 71.2 μM). Consequently, none were selective inhibitors of SARS-CoV replication (SI values <1-3.3 μM). These data portended the poor efficacy of promazine in a SARS-CoV mouse lung replication model. Intraperitoneal treatment with promazine using a prophylactic (-4 h)/therapeutic regimen of 1, 10, or 50 mg/(kg day) did not reduce virus lung titers at day 3, yet prolonged virus replication to 14 days. Similar therapeutic promazine doses were not efficacious. Thus, promazine did not affect SARS-CoV replication in vitro or in vivo, nor were any other phenothiazines efficacious in reducing virus replication. Therefore, treating SARS infections with compounds like promazine is not warranted.</div>
</front>
</TEI>
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<s3>HKG</s3>
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<placeName><settlement type="city">Sha Tin</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sidwell, Robert W" sort="Sidwell, Robert W" uniqKey="Sidwell R" first="Robert W." last="Sidwell">Robert W. Sidwell</name>
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</placeName>
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</author>
</analytic>
<series><title level="j" type="main">Antiviral research</title>
<title level="j" type="abbreviated">Antivir. res.</title>
<idno type="ISSN">0166-3542</idno>
<imprint><date when="2008">2008</date>
</imprint>
</series>
</biblStruct>
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<seriesStmt><title level="j" type="main">Antiviral research</title>
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<term>Antipsychotic</term>
<term>Antiviral</term>
<term>Mouse</term>
<term>Neuroleptic</term>
<term>Promazine</term>
<term>Psychotropic</term>
<term>Replication</term>
<term>Severe acute respiratory syndrome</term>
<term>Severe acute respiratory syndrome virus</term>
<term>Structure activity relation</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Antipsychotique</term>
<term>Neuroleptique</term>
<term>Relation structure activité</term>
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<term>Syndrome respiratoire aigu sévère</term>
<term>Virus syndrome respiratoire aigu sévère</term>
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<term>Modèle animal</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Phenothiazine and derivatives were tested for inhibition of SARS-CoV replication. Phenothiazine slightly inhibited SARS-CoV replication in a neutral red (NR) uptake assay. Adding a propylamino group to give promazine reduced virus yields (VYR assay) with an EC<sub>90</sub>
 = 8.3 ± 2.8 μM, but without selectivity. Various substitutions in the basic phenothiazine structure did not promote efficacy. Phenazine ethosulfate was the most potent compound by VYR assay (EC<sub>90</sub>
 = 6.1 ± 4.3 μM). All compounds were toxic (IC<sub>50</sub>
 = 6.6-74.5 μM) except for phenoxathiin (IC<sub>50</sub>
 = 858 ± 208 μM) and 10-(alpha-diethylamino-propionyl) phenothiazine.HCl (IC<sub>50</sub>
 =195 ± 71.2 μM). Consequently, none were selective inhibitors of SARS-CoV replication (SI values <1-3.3 μM). These data portended the poor efficacy of promazine in a SARS-CoV mouse lung replication model. Intraperitoneal treatment with promazine using a prophylactic (-4 h)/therapeutic regimen of 1, 10, or 50 mg/(kg day) did not reduce virus lung titers at day 3, yet prolonged virus replication to 14 days. Similar therapeutic promazine doses were not efficacious. Thus, promazine did not affect SARS-CoV replication in vitro or in vivo, nor were any other phenothiazines efficacious in reducing virus replication. Therefore, treating SARS infections with compounds like promazine is not warranted.</div>
</front>
</TEI>
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<author><name sortKey="Lauridsen, Larry" sort="Lauridsen, Larry" uniqKey="Lauridsen L" first="Larry" last="Lauridsen">Larry Lauridsen</name>
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</author>
<author><name sortKey="Jung, Kie Hoon" sort="Jung, Kie Hoon" uniqKey="Jung K" first="Kie-Hoon" last="Jung">Kie-Hoon Jung</name>
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<author><name sortKey="Li, Joseph K K" sort="Li, Joseph K K" uniqKey="Li J" first="Joseph K.-K." last="Li">Joseph K.-K. Li</name>
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<author><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K. S." last="Chan">Paul K. S. Chan</name>
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<placeName><settlement type="city">Sha Tin</settlement>
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<term>Antiviral Agents (pharmacology)</term>
<term>Antiviral Agents (therapeutic use)</term>
<term>Antiviral Agents (toxicity)</term>
<term>Cell Survival</term>
<term>Chemoprevention</term>
<term>Chlorocebus aethiops</term>
<term>Cytokines (analysis)</term>
<term>Female</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Molecular Structure</term>
<term>Neutral Red (metabolism)</term>
<term>Phenothiazines (administration & dosage)</term>
<term>Phenothiazines (pharmacology)</term>
<term>Phenothiazines (therapeutic use)</term>
<term>Phenothiazines (toxicity)</term>
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<term>Cytokines (analyse)</term>
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<term>Phénothiazines (pharmacologie)</term>
<term>Phénothiazines (toxicité)</term>
<term>Phénothiazines (usage thérapeutique)</term>
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<term>Poumon (virologie)</term>
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<term>Souris de lignée BALB C</term>
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<term>Syndrome respiratoire aigu sévère ()</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antiviraux</term>
<term>Phénothiazines</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Survival</term>
<term>Chemoprevention</term>
<term>Chlorocebus aethiops</term>
<term>Female</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Molecular Structure</term>
<term>Vero Cells</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules Vero</term>
<term>Chimioprévention</term>
<term>Femelle</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Structure moléculaire</term>
<term>Survie cellulaire</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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</profileDesc>
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<front><div type="abstract" xml:lang="en"><p>Phenothiazine and derivatives were tested for inhibition of SARS-CoV replication. Phenothiazine slightly inhibited SARS-CoV replication in a neutral red (NR) uptake assay. Adding a propylamino group to give promazine reduced virus yields (VYR assay) with an EC<sub>90</sub>
 = 8.3 ± 2.8 μM, but without selectivity. Various substitutions in the basic phenothiazine structure did not promote efficacy. Phenazine ethosulfate was the most potent compound by VYR assay (EC<sub>90</sub>
 = 6.1 ± 4.3 μM). All compounds were toxic (IC<sub>50</sub>
 = 6.6–74.5 μM) except for phenoxathiin (IC<sub>50</sub>
 = 858 ± 208 μM) and 10-(alpha-diethylamino-propionyl) phenothiazine·HCl (IC<sub>50</sub>
 = 195 ± 71.2 μM). Consequently, none were selective inhibitors of SARS-CoV replication (SI values <1–3.3 μM). These data portended the poor efficacy of promazine in a SARS-CoV mouse lung replication model. Intraperitoneal treatment with promazine using a prophylactic (−4 h)/therapeutic regimen of 1, 10, or 50 mg/(kg day) did not reduce virus lung titers at day 3, yet prolonged virus replication to 14 days. Similar therapeutic promazine doses were not efficacious. Thus, promazine did not affect SARS-CoV replication in vitro or in vivo, nor were any other phenothiazines efficacious in reducing virus replication. Therefore, treating SARS infections with compounds like promazine is not warranted.</p>
</div>
</front>
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   |area=    SrasV1
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   |texte=   Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model
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Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model

Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model

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