valnoctamide  (Millipore)


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    Valnoctamide
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    v4765
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    Structured Review

    Millipore valnoctamide
    Valnoctamide

    https://www.bioz.com/result/valnoctamide/product/Millipore
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    valnoctamide - by Bioz Stars, 2020-09
    91/100 stars

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    1) Product Images from "Valnoctamide Inhibits Cytomegalovirus Infection in Developing Brain and Attenuates Neurobehavioral Dysfunctions and Brain Abnormalities"

    Article Title: Valnoctamide Inhibits Cytomegalovirus Infection in Developing Brain and Attenuates Neurobehavioral Dysfunctions and Brain Abnormalities

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0970-17.2017

    Valnoctamide reverses deficient brain growth induced by mCMV infection. A , Photograph shows decreased brain size in an infected, untreated mouse (i.e., mCMV; middle) compared with an uninfected control (left). VCD treatment restores normal brain growth (mCMV+VCD, right). Quantification of VCD-mediated benefits on postnatal brain growth by calculation of brain-to-body weight ratio. Values are reported as the mean ± SEM; n = 10 mice/group (3 litters). ns, Not significant. ** p
    Figure Legend Snippet: Valnoctamide reverses deficient brain growth induced by mCMV infection. A , Photograph shows decreased brain size in an infected, untreated mouse (i.e., mCMV; middle) compared with an uninfected control (left). VCD treatment restores normal brain growth (mCMV+VCD, right). Quantification of VCD-mediated benefits on postnatal brain growth by calculation of brain-to-body weight ratio. Values are reported as the mean ± SEM; n = 10 mice/group (3 litters). ns, Not significant. ** p

    Techniques Used: Infection, Mouse Assay

    Valnoctamide suppresses mCMV load in the brain of mice infected intraperitoneally on the day of birth. Newborn mice were infected at P0 with 750 pfu of mCMV intraperitoneally and were randomized to receive either vehicle (mCMV+VEH) or VCD (mCMV+VCD) subcutaneously from P1 until P21. A–E , Viral load was quantified in the cerebrum ( A ), cerebellum ( B ), whole blood ( C ), liver ( D ), and spleen ( E ) by qRT-PCR at the specified time points and were expressed as log 10 genome copies per gram/ml harvested tissue/blood. Data are presented as the mean ± SEM; n = 7–10 mice/time point. Viral titers below the limit of detection (LoD, dotted line) were plotted as 2 log 10 genome copies. ns, Not significant. * p
    Figure Legend Snippet: Valnoctamide suppresses mCMV load in the brain of mice infected intraperitoneally on the day of birth. Newborn mice were infected at P0 with 750 pfu of mCMV intraperitoneally and were randomized to receive either vehicle (mCMV+VEH) or VCD (mCMV+VCD) subcutaneously from P1 until P21. A–E , Viral load was quantified in the cerebrum ( A ), cerebellum ( B ), whole blood ( C ), liver ( D ), and spleen ( E ) by qRT-PCR at the specified time points and were expressed as log 10 genome copies per gram/ml harvested tissue/blood. Data are presented as the mean ± SEM; n = 7–10 mice/time point. Viral titers below the limit of detection (LoD, dotted line) were plotted as 2 log 10 genome copies. ns, Not significant. * p

    Techniques Used: Mouse Assay, Infection, Quantitative RT-PCR

    Subcutaneously injected valnoctamide enters the brain and suppresses mCMV replication within the brain. Quantification of mCMV load in the brain of mice intracranially infected with 2 × 10 4 pfu of mCMV on day 3 after birth. The amount of virus in the cerebrum (left) and the cerebellum (right) was calculated by qRT-PCR in P9 mice receiving either vehicle (VEH) or VCD subcutaneously from P3 through P8 and expressed as genome copies per gram of harvested tissue. Values are reported as the mean ± SEM; n = 8 mice/time-point. ** p
    Figure Legend Snippet: Subcutaneously injected valnoctamide enters the brain and suppresses mCMV replication within the brain. Quantification of mCMV load in the brain of mice intracranially infected with 2 × 10 4 pfu of mCMV on day 3 after birth. The amount of virus in the cerebrum (left) and the cerebellum (right) was calculated by qRT-PCR in P9 mice receiving either vehicle (VEH) or VCD subcutaneously from P3 through P8 and expressed as genome copies per gram of harvested tissue. Values are reported as the mean ± SEM; n = 8 mice/time-point. ** p

    Techniques Used: Injection, Mouse Assay, Infection, Quantitative RT-PCR

    Impaired cerebellar-mediated motor functions in mCMV-infected mice are ameliorated by valnoctamide treatment. A , Photographs display stereotypical clasping response with hindlimbs retracted to the abdomen in an mCMV-infected mouse (middle), and a normal response with splayed out hindlimbs in an uninfected control (left) and in an mCMV-infected, VCD-treated animal (right). B , Scoring of clasping response according to hindlimb position. C , Increased T LA in infected, untreated mice in the vertical pole test, compared with VCD-treated infected animals and uninfected controls. D , E , Investigation of fine motor coordination and balance by challenging beam traversal test. Infected mice need more time to traverse the beam ( D ) and slip more ( E ) than the control mice. Both aspects are improved by VCD administration. Values are reported as the mean ± SEM; n = 10–13 mice/group. * p
    Figure Legend Snippet: Impaired cerebellar-mediated motor functions in mCMV-infected mice are ameliorated by valnoctamide treatment. A , Photographs display stereotypical clasping response with hindlimbs retracted to the abdomen in an mCMV-infected mouse (middle), and a normal response with splayed out hindlimbs in an uninfected control (left) and in an mCMV-infected, VCD-treated animal (right). B , Scoring of clasping response according to hindlimb position. C , Increased T LA in infected, untreated mice in the vertical pole test, compared with VCD-treated infected animals and uninfected controls. D , E , Investigation of fine motor coordination and balance by challenging beam traversal test. Infected mice need more time to traverse the beam ( D ) and slip more ( E ) than the control mice. Both aspects are improved by VCD administration. Values are reported as the mean ± SEM; n = 10–13 mice/group. * p

    Techniques Used: Infection, Mouse Assay

    Delayed acquisition of neurological milestones induced by mCMV infection is completely rescued by valnoctamide therapy. A–H , Graphs show neurodevelopmental delays in mCMV-infected pups (solid gray triangles) as assessed by the righting reflex ( A ), the cliff aversion ( B ), the forelimb grasping and placing reflex ( C , D ), the negative geotaxis ( E ), the level screen test ( F ), the screen climbing test ( G ), and the vibrissa placing reflex ( H ; for a detailed description, see Materials and Methods). VCD-treated animals (solid green triangles) showed neurological responses similar to uninfected controls receiving either vehicle (VEH; empty gray circles) or VCD (empty green circles). Values are reported as the mean ± SEM, n = 20–24 mice (9–12 males)/experimental group. ns, Not significant. * p
    Figure Legend Snippet: Delayed acquisition of neurological milestones induced by mCMV infection is completely rescued by valnoctamide therapy. A–H , Graphs show neurodevelopmental delays in mCMV-infected pups (solid gray triangles) as assessed by the righting reflex ( A ), the cliff aversion ( B ), the forelimb grasping and placing reflex ( C , D ), the negative geotaxis ( E ), the level screen test ( F ), the screen climbing test ( G ), and the vibrissa placing reflex ( H ; for a detailed description, see Materials and Methods). VCD-treated animals (solid green triangles) showed neurological responses similar to uninfected controls receiving either vehicle (VEH; empty gray circles) or VCD (empty green circles). Values are reported as the mean ± SEM, n = 20–24 mice (9–12 males)/experimental group. ns, Not significant. * p

    Techniques Used: Infection, Mouse Assay

    Valnoctamide substantially ameliorates cerebellar development in mCMV-infected mice. A , Photomicrograph of representative fluorescent Nissl-stained cerebellar areas in control (left) and infected mice with (right, mCMV+VCD) or without (middle, mCMV) VCD. Note the delayed foliation in infected, untreated cerebellum, rescued by VCD. Scale bar, 200 μm. B , Graph depicts cerebellar area, expressed as a percentage of total brain area (three sagittal sections/animal, five animals/group). C , Photomicrograph showing cerebellar PCs and ML by means of calbindin D-28K staining. Infected, untreated cerebellum (middle) displays loss of PCs and thinner ML compared with uninfected control (left); VCD improves both parameters (right). Scale bar, 200 μm. D–F , Quantification of PC number ( D ), and ML ( E ) and IGL thickness ( F ) along 500 μm of the primary fissure (prf; both sides; three sagittal sections/mouse, five mice/group). G , Fluorescent micrograph of heterotopic PCs (arrowheads) identified in an infected untreated cerebellum. Scale bar, 100 μm. H , Photomicrograph displays pathological persistence of EGL in mCMV-infected, untreated cerebellum at P30 (middle); no EGL could be identified at the same time point in uninfected control (left) and infected, VCD-treated cerebellum (right). Scale bar, 200 μm. Values are reported as the mean ± SEM. ns, Not significant. * p
    Figure Legend Snippet: Valnoctamide substantially ameliorates cerebellar development in mCMV-infected mice. A , Photomicrograph of representative fluorescent Nissl-stained cerebellar areas in control (left) and infected mice with (right, mCMV+VCD) or without (middle, mCMV) VCD. Note the delayed foliation in infected, untreated cerebellum, rescued by VCD. Scale bar, 200 μm. B , Graph depicts cerebellar area, expressed as a percentage of total brain area (three sagittal sections/animal, five animals/group). C , Photomicrograph showing cerebellar PCs and ML by means of calbindin D-28K staining. Infected, untreated cerebellum (middle) displays loss of PCs and thinner ML compared with uninfected control (left); VCD improves both parameters (right). Scale bar, 200 μm. D–F , Quantification of PC number ( D ), and ML ( E ) and IGL thickness ( F ) along 500 μm of the primary fissure (prf; both sides; three sagittal sections/mouse, five mice/group). G , Fluorescent micrograph of heterotopic PCs (arrowheads) identified in an infected untreated cerebellum. Scale bar, 100 μm. H , Photomicrograph displays pathological persistence of EGL in mCMV-infected, untreated cerebellum at P30 (middle); no EGL could be identified at the same time point in uninfected control (left) and infected, VCD-treated cerebellum (right). Scale bar, 200 μm. Values are reported as the mean ± SEM. ns, Not significant. * p

    Techniques Used: Infection, Mouse Assay, Staining

    2) Product Images from "Mood stabilizers inhibit cytomegalovirus infection"

    Article Title: Mood stabilizers inhibit cytomegalovirus infection

    Journal: Virology

    doi: 10.1016/j.virol.2016.09.012

    Valpromide and valnoctamide substantially decrease CMV load in target organs ( A ) A small number of cells show CMV infection in the liver of PND 12 mice infected on DOB and treated daily with VCD until PND 10 (left); in contrast, a higher number was commonly found in the liver of pups receiving vehicle (right). GFP-positive cells are localized both in the parenchyma (arrows) and in the sub-peritoneal area (arrowheads). Asterisks indicate lobule central veins. Scale 100 µm. ( B to D ) Infected newborns treated with VPD, VCD, or VEH from PND 1 to 10, were euthanized at PND 12, and tissue samples from liver, spleen, and lungs were collected for measurement of viral titer by plaque assay. Bar graphs show titers as PFU/mg of tissue; mean ± SEM; N=6 mice/group; *** p
    Figure Legend Snippet: Valpromide and valnoctamide substantially decrease CMV load in target organs ( A ) A small number of cells show CMV infection in the liver of PND 12 mice infected on DOB and treated daily with VCD until PND 10 (left); in contrast, a higher number was commonly found in the liver of pups receiving vehicle (right). GFP-positive cells are localized both in the parenchyma (arrows) and in the sub-peritoneal area (arrowheads). Asterisks indicate lobule central veins. Scale 100 µm. ( B to D ) Infected newborns treated with VPD, VCD, or VEH from PND 1 to 10, were euthanized at PND 12, and tissue samples from liver, spleen, and lungs were collected for measurement of viral titer by plaque assay. Bar graphs show titers as PFU/mg of tissue; mean ± SEM; N=6 mice/group; *** p

    Techniques Used: Infection, Mouse Assay, Plaque Assay

    Valnoctamide blocks mouse and human CMV ( A ) Chemical structure of valnoctamide. ( B ) Microscopic fields show GFP fluorescence (top) and phase contrast (bottom) of NIH/3T3 cells pre-treated (24hrs) with VCD (1mM) or vehicle prior to inoculation with mCMV (MOI 0.03). Photos captured 48 hpi; scale 50 µm. ( C to F ) VCD-mediated dose-dependent decrease in mCMV infection at low MOI (0.03, C to E) and high MOI (4, F) in NIH/3T3 cells (C, D, and F) and neuro-2a (E) as assessed by counting infected GFP-positive cells at 48 hpi (C to E) and viral yield assay at 72 hpi (F); other conditions same as B. ( G ) Dose-response analysis in NIH/3T3 cells pre-treated with VCD for 24 hours, infected with mCMV-GFP (MOI 0.03), and incubated for 4 days before viral fluorescent plaques counting. The EC 50 is shown. Mean ± SEM of 2 independent experiments. ( H ) The potential cytotoxic effect of VCD at 1 and 10 mM on uninfected NIH/3T3 after 24 and 72 hours of exposure was assessed by the red fluorescent EthD-1 assay and results compared with vehicle (VEH) at the same concentrations and plain media. ( I to L ) VCD-mediated decrease in hCMV infection at low MOI (0.01, I and J) and high MOI (1, K and L) in human dermal fibroblasts, evaluated by GFP-positive cells counting at 48 hpi (K) or 72 hpi (I) and viral yield assay at 96 hpi (J and L). Mean ± SEM of 8 (C to E, and H to J) and 6 (F, K, and L) cultures; ns, not significant, * p
    Figure Legend Snippet: Valnoctamide blocks mouse and human CMV ( A ) Chemical structure of valnoctamide. ( B ) Microscopic fields show GFP fluorescence (top) and phase contrast (bottom) of NIH/3T3 cells pre-treated (24hrs) with VCD (1mM) or vehicle prior to inoculation with mCMV (MOI 0.03). Photos captured 48 hpi; scale 50 µm. ( C to F ) VCD-mediated dose-dependent decrease in mCMV infection at low MOI (0.03, C to E) and high MOI (4, F) in NIH/3T3 cells (C, D, and F) and neuro-2a (E) as assessed by counting infected GFP-positive cells at 48 hpi (C to E) and viral yield assay at 72 hpi (F); other conditions same as B. ( G ) Dose-response analysis in NIH/3T3 cells pre-treated with VCD for 24 hours, infected with mCMV-GFP (MOI 0.03), and incubated for 4 days before viral fluorescent plaques counting. The EC 50 is shown. Mean ± SEM of 2 independent experiments. ( H ) The potential cytotoxic effect of VCD at 1 and 10 mM on uninfected NIH/3T3 after 24 and 72 hours of exposure was assessed by the red fluorescent EthD-1 assay and results compared with vehicle (VEH) at the same concentrations and plain media. ( I to L ) VCD-mediated decrease in hCMV infection at low MOI (0.01, I and J) and high MOI (1, K and L) in human dermal fibroblasts, evaluated by GFP-positive cells counting at 48 hpi (K) or 72 hpi (I) and viral yield assay at 96 hpi (J and L). Mean ± SEM of 8 (C to E, and H to J) and 6 (F, K, and L) cultures; ns, not significant, * p

    Techniques Used: Fluorescence, Infection, Incubation, Ethidium Homodimer Assay

    Valpromide and valnoctamide safely improve survival and postnatal body growth of infected newborns ( A ) Uninfected pups received 20 µL of saline (CTR), vehicle (VEH), VPD, or VCD (1.4 mg/mL), once a day, subcutaneously, from PND 1 to PND 21, when the body weight was assessed. Mean ± SEM, one-way ANOVA with Bonferroni’s post-hoc test; N=8 mice/experimental group. ( B ) Timeline showing mCMV infection of neonates and compounds administration. ( C ) Survival at PND 49 assessed by Log-rank (Mantel-Cox) test; N=11–13 mice/group. ( D to G ) Drug-induced improvement in postnatal body growth. Photo shows enhanced body size of VPD- and VCD-treated pups compared to vehicle (mCMV) (D). Graphs show postnatal body weight (E), body length (F), and tail length (G) increase from DOB to PND 20. CTR, control/uninfected mice treated with saline; VPD, VCD, and VEH, infected newborns treated with the indicated compounds. Mean ± SEM; error bars shown for VEH group; N=6–9 mice/group; mixed-model ANOVA (Newman Keuls test) for VPD and VCD versus CTR (E) and for VPD and VCD versus VEH (E to G); * p
    Figure Legend Snippet: Valpromide and valnoctamide safely improve survival and postnatal body growth of infected newborns ( A ) Uninfected pups received 20 µL of saline (CTR), vehicle (VEH), VPD, or VCD (1.4 mg/mL), once a day, subcutaneously, from PND 1 to PND 21, when the body weight was assessed. Mean ± SEM, one-way ANOVA with Bonferroni’s post-hoc test; N=8 mice/experimental group. ( B ) Timeline showing mCMV infection of neonates and compounds administration. ( C ) Survival at PND 49 assessed by Log-rank (Mantel-Cox) test; N=11–13 mice/group. ( D to G ) Drug-induced improvement in postnatal body growth. Photo shows enhanced body size of VPD- and VCD-treated pups compared to vehicle (mCMV) (D). Graphs show postnatal body weight (E), body length (F), and tail length (G) increase from DOB to PND 20. CTR, control/uninfected mice treated with saline; VPD, VCD, and VEH, infected newborns treated with the indicated compounds. Mean ± SEM; error bars shown for VEH group; N=6–9 mice/group; mixed-model ANOVA (Newman Keuls test) for VPD and VCD versus CTR (E) and for VPD and VCD versus VEH (E to G); * p

    Techniques Used: Infection, Mouse Assay

    Valpromide and valnoctamide inhibit hCMV attachment to cell ( A ). HDF cells infected with hCMV-GFP (MOI 0.01) (t=0) were exposed to VPD, VCD, or vehicle (100 µM) simultaneously, or 2 or 12 hours after virus inoculation until media collection at 96 hpi. Viral replication assessed by titer determination using a plaque assay on HDF monolayers. ( B ) A drug (100 µM)/undiluted hCMV mixture was incubated for 2 hours at 37°C or 4°C. Before cell inoculation, the solution was diluted to 10 nM (ineffective drug concentration). ( C ) Human fibroblasts infected with hCMV (MOI 0.01) and treated with the compounds (100 µM) starting from viral challenge (t=0) or 2 hpi, were fixed and permeabilized at 8 hpi for immunofluorescence with anti-IE1/2 monoclonal antibody and DAPI staining. Scale bar 100 µm. ( D and E ) Attachment and fusion assays were performed as described in Materials and Methods. GFP-positive cells were counted at 72 hpi (D). Results presented as the fold change (2 −ΔΔCT ) of hCMV DNA in each experimental condition relative to vehicle (mean ± SEM of 2 biological replicates) (E). ( F ) Plaque reduction assay on HDF cells exposed to vehicle, GCV (100 nM), VCD (1 µM), HS (25 µg/mL – 40 µM), or a combination of these compounds as indicated for 24 hours before hCMV inoculation (MOI 0.01). Fluorescent plaques counted at 7 dpi. The mean plaque counts for each drug were expressed as a percentage of the control (vehicle) mean plaque count, defined as 100%; p
    Figure Legend Snippet: Valpromide and valnoctamide inhibit hCMV attachment to cell ( A ). HDF cells infected with hCMV-GFP (MOI 0.01) (t=0) were exposed to VPD, VCD, or vehicle (100 µM) simultaneously, or 2 or 12 hours after virus inoculation until media collection at 96 hpi. Viral replication assessed by titer determination using a plaque assay on HDF monolayers. ( B ) A drug (100 µM)/undiluted hCMV mixture was incubated for 2 hours at 37°C or 4°C. Before cell inoculation, the solution was diluted to 10 nM (ineffective drug concentration). ( C ) Human fibroblasts infected with hCMV (MOI 0.01) and treated with the compounds (100 µM) starting from viral challenge (t=0) or 2 hpi, were fixed and permeabilized at 8 hpi for immunofluorescence with anti-IE1/2 monoclonal antibody and DAPI staining. Scale bar 100 µm. ( D and E ) Attachment and fusion assays were performed as described in Materials and Methods. GFP-positive cells were counted at 72 hpi (D). Results presented as the fold change (2 −ΔΔCT ) of hCMV DNA in each experimental condition relative to vehicle (mean ± SEM of 2 biological replicates) (E). ( F ) Plaque reduction assay on HDF cells exposed to vehicle, GCV (100 nM), VCD (1 µM), HS (25 µg/mL – 40 µM), or a combination of these compounds as indicated for 24 hours before hCMV inoculation (MOI 0.01). Fluorescent plaques counted at 7 dpi. The mean plaque counts for each drug were expressed as a percentage of the control (vehicle) mean plaque count, defined as 100%; p

    Techniques Used: Infection, Plaque Assay, Incubation, Concentration Assay, Immunofluorescence, Staining

    Daily valpromide and valnoctamide administration ameliorates postnatal somatic development ( A to F ) Graphs show progressive improvement of multiple parameters of postnatal growth. Mean ± SEM; error bars not shown for clarity. N=6–9 mice/group; mixed-model ANOVA (Newman Keuls test) for VPD and VCD versus VEH; ** p
    Figure Legend Snippet: Daily valpromide and valnoctamide administration ameliorates postnatal somatic development ( A to F ) Graphs show progressive improvement of multiple parameters of postnatal growth. Mean ± SEM; error bars not shown for clarity. N=6–9 mice/group; mixed-model ANOVA (Newman Keuls test) for VPD and VCD versus VEH; ** p

    Techniques Used: Mouse Assay