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minzasolmin  (MedChemExpress)


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    Structured Review

    MedChemExpress minzasolmin
    (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered <t>Minzasolmin</t> (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.
    Minzasolmin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    Images

    1) Product Images from "Ser129 Phosphorylation Paradox: Non-phosphorylated α-Synuclein Drives Parkinson’s Disease-like Pathogenesis in Vivo"

    Article Title: Ser129 Phosphorylation Paradox: Non-phosphorylated α-Synuclein Drives Parkinson’s Disease-like Pathogenesis in Vivo

    Journal: bioRxiv

    doi: 10.64898/2025.12.21.695762

    (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered Minzasolmin (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.
    Figure Legend Snippet: (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered Minzasolmin (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.

    Techniques Used: Injection, Phospho-proteomics, Plasmid Preparation, Control, Virus, Knock-In



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    MedChemExpress minzasolmin
    (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered <t>Minzasolmin</t> (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.
    Minzasolmin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered <t>Minzasolmin</t> (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.
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    Charles River Laboratories minzasolmin captisol
    The structure, IUPAC nomenclature and molecular weight of <t>minzasolmin</t> (International Patent Publication Number WO 2015/116663 A1). The rendering was generated by Biovia Draw 2020 version 20.1.
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    Image Search Results


    (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered Minzasolmin (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.

    Journal: bioRxiv

    Article Title: Ser129 Phosphorylation Paradox: Non-phosphorylated α-Synuclein Drives Parkinson’s Disease-like Pathogenesis in Vivo

    doi: 10.64898/2025.12.21.695762

    Figure Lengend Snippet: (A) Schematic of experimental design for assessing aging-related symptoms in WT, S129A homozygous (S129A + / + ), and heterozygous (S129A + / − ) mice. (B) Relative change in food-finding latency across genotypes (n=13-25). (C) Relative change in fecal weight across genotypes (n=6-14). (D) Relative change in fecal water content across genotypes (n=6-14). (E) 1-month-old WT and S129A + / + mice injected with AAV-S129D (to restore S129 phosphorylation) or AAV-Vector (control), followed by aging-related behavioral assessments. (F) Food-finding latency in AAV-treated mice (n=6-12). (G) Fecal weight in AAV-treated mice (n=10). (H) Fecal water content in AAV-treated mice (n=10). (I) 1-month-old S129A + / + mice administered Minzasolmin (α-syn aggregation inhibitor) or Captisol (vehicle), followed by aging-related behavioral assessments. (J) Food-finding latency in Minzasolmin/vehicle-treated S129A + / + mice (n=per group sample size). (K) Fecal weight in Minzasolmin/vehicle-treated S129A + / + mice (n=5-7). (L) Fecal water content in Minzasolmin/vehicle-treated S129A + / + mice (n=8). All data are presented as mean ± SEM. Statistical analyses used one-way ANOVA with Tukey’s post hoc test. AAV, adeno-associated virus; KI, knock-in; WT, wild-type.

    Article Snippet: Minzasolmin (UCB0599, MedChemExpress, NJ, USA) was dissolved in a vehicle solution containing 40% Captisol (Aladdin, Shanghai, China) in sterile water.

    Techniques: Injection, Phospho-proteomics, Plasmid Preparation, Control, Virus, Knock-In

    The structure, IUPAC nomenclature and molecular weight of minzasolmin (International Patent Publication Number WO 2015/116663 A1). The rendering was generated by Biovia Draw 2020 version 20.1.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: The structure, IUPAC nomenclature and molecular weight of minzasolmin (International Patent Publication Number WO 2015/116663 A1). The rendering was generated by Biovia Draw 2020 version 20.1.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Molecular Weight, Generated

    Pharmacokinetic parameters of  minzasolmin  in C57/Bl6 mice following single dose intraperitoneal administration of 1 or 5 mg/kg.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: Pharmacokinetic parameters of minzasolmin in C57/Bl6 mice following single dose intraperitoneal administration of 1 or 5 mg/kg.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques:

    a Line 61 transgenic mice had gait deficits as indicated by lower round beam performance composite scores in vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice (****P < 0.0001; N/group = 8 (Non-tg/Vehicle), 9 (Line 61 tg/Vehicle), 11 (Line 61 tg/1 mg/kg) and 10 (Line 61 tg/5 mg/kg)). Gait deficits were attenuated in 1 mg/kg minzasolmin (UCB0599)-treated Line 61 transgenic mice compared to vehicle-treated Line 61 transgenic mice with an increase in scoring ( ## P < 0.01). Data are presented as group means ± SEM. b Radar plot of composite score components used to visualize the gait and balance-related deficit profile of vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice that is normalized by minzasolmin treatments.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: a Line 61 transgenic mice had gait deficits as indicated by lower round beam performance composite scores in vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice (****P < 0.0001; N/group = 8 (Non-tg/Vehicle), 9 (Line 61 tg/Vehicle), 11 (Line 61 tg/1 mg/kg) and 10 (Line 61 tg/5 mg/kg)). Gait deficits were attenuated in 1 mg/kg minzasolmin (UCB0599)-treated Line 61 transgenic mice compared to vehicle-treated Line 61 transgenic mice with an increase in scoring ( ## P < 0.01). Data are presented as group means ± SEM. b Radar plot of composite score components used to visualize the gait and balance-related deficit profile of vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice that is normalized by minzasolmin treatments.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Transgenic Assay, Control

    Proteinase K-resistant ASYN immunolabeling was observed in the ( a ) cortex, ( b ) hippocampus and ( c ) striatum of vehicle-treated Line 61 transgenic, but not non-transgenic control mice. Compared to vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant reductions in total ASYN levels in the ( a ) cortex ( b ) hippocampus, and ( c ) striatum ( #### P < 0.0001 , for all regions and doses) . Data are presented as group means ± SEM. Representative images in ( d ) were chosen based on the group mean for each treatment group. Scale bars represent 250 μm and 40 μm for low- and high-magnification images, respectively.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: Proteinase K-resistant ASYN immunolabeling was observed in the ( a ) cortex, ( b ) hippocampus and ( c ) striatum of vehicle-treated Line 61 transgenic, but not non-transgenic control mice. Compared to vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant reductions in total ASYN levels in the ( a ) cortex ( b ) hippocampus, and ( c ) striatum ( #### P < 0.0001 , for all regions and doses) . Data are presented as group means ± SEM. Representative images in ( d ) were chosen based on the group mean for each treatment group. Scale bars represent 250 μm and 40 μm for low- and high-magnification images, respectively.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Immunolabeling, Transgenic Assay, Control, Produced

    Statistically significant increases in total ASYN immunolabeling were observed in the ( a ) cortex, ( b ) hippocampus and ( c ) striatum of vehicle-treated Line 61 transgenic mice as compared to non-transgenic control mice ( ****P < 0.0001 for all regions). Compared with vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant reductions in total ASYN levels in the ( a ) cortex ( # P < 0.05 and #### P < 0.0001, respectively), ( b ) hippocampus ( #### P < 0.0001, for both doses), and ( c ) striatum ( #### P < 0.0001, for both doses) . Data are presented as group means ± SEM. Representative images in ( d ) were chosen based on the group mean for each treatment group. Scale bars represent 250 μm and 40 μm for low- and high-magnification images, respectively.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: Statistically significant increases in total ASYN immunolabeling were observed in the ( a ) cortex, ( b ) hippocampus and ( c ) striatum of vehicle-treated Line 61 transgenic mice as compared to non-transgenic control mice ( ****P < 0.0001 for all regions). Compared with vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant reductions in total ASYN levels in the ( a ) cortex ( # P < 0.05 and #### P < 0.0001, respectively), ( b ) hippocampus ( #### P < 0.0001, for both doses), and ( c ) striatum ( #### P < 0.0001, for both doses) . Data are presented as group means ± SEM. Representative images in ( d ) were chosen based on the group mean for each treatment group. Scale bars represent 250 μm and 40 μm for low- and high-magnification images, respectively.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Immunolabeling, Transgenic Assay, Control, Produced

    Evaluations of dopamine transporter levels in striatum. a Statistically significant decreases in striatal DAT immunolabeling were observed in vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice (**** P < 0.0001). Compared with vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant normalizations in striatal DAT levels ( # P < 0.05 and #### P < 0.0001, respectively). Data are presented as group means ± SEM. Representative images in ( b ) were chosen based on the group mean for each treatment group. Low magnification survey images were obtained at 4x and followed by imaging at ×40 for analysis of DAT immunolabeling (scale bar = 25 mm). c Pearson r correlation analyses of DAT with (left to right panels) total or Proteinase K-resistant forms of ASYN in the striatum, or functional round beam composite scoring reveals negative and positive correlations, respectively.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: Evaluations of dopamine transporter levels in striatum. a Statistically significant decreases in striatal DAT immunolabeling were observed in vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice (**** P < 0.0001). Compared with vehicle-treated Line 61 transgenic controls, minzasolmin (UCB0599) administration (1 and 5 mg/kg) in Line 61 transgenic mice produced statistically significant normalizations in striatal DAT levels ( # P < 0.05 and #### P < 0.0001, respectively). Data are presented as group means ± SEM. Representative images in ( b ) were chosen based on the group mean for each treatment group. Low magnification survey images were obtained at 4x and followed by imaging at ×40 for analysis of DAT immunolabeling (scale bar = 25 mm). c Pearson r correlation analyses of DAT with (left to right panels) total or Proteinase K-resistant forms of ASYN in the striatum, or functional round beam composite scoring reveals negative and positive correlations, respectively.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Immunolabeling, Transgenic Assay, Control, Produced, Imaging, Functional Assay

    GFAP immunolabeling was increased in the ( a ) neocortex and ( b ) hippocampus (CA1/2) of vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice ( **** P < 0.0001 , for both regions ). 1 and 5 mg/kg minzasolmin administration decreased GFAP immunolabeling in Line 61 transgenic mice compared to vehicle-treated Line 61 transgenic mice ( #### P < 0.0001 , for both regions and doses) . Data are presented as group means ± SEM. Representative images in ( c ) were chosen based on the group mean for each treatment group. A low-magnification overview of the hippocampus and overlying cortical regions is shown in the upper row of images. Higher-magnification inset images of GFAP immunolabeling in the hippocampus are shown in the lower row of images. d There were positive correlations between GFAP with total ASYN in the cortex (left panel), and the hippocampus (right panel).

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: GFAP immunolabeling was increased in the ( a ) neocortex and ( b ) hippocampus (CA1/2) of vehicle-treated Line 61 transgenic mice compared to non-transgenic control mice ( **** P < 0.0001 , for both regions ). 1 and 5 mg/kg minzasolmin administration decreased GFAP immunolabeling in Line 61 transgenic mice compared to vehicle-treated Line 61 transgenic mice ( #### P < 0.0001 , for both regions and doses) . Data are presented as group means ± SEM. Representative images in ( c ) were chosen based on the group mean for each treatment group. A low-magnification overview of the hippocampus and overlying cortical regions is shown in the upper row of images. Higher-magnification inset images of GFAP immunolabeling in the hippocampus are shown in the lower row of images. d There were positive correlations between GFAP with total ASYN in the cortex (left panel), and the hippocampus (right panel).

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Immunolabeling, Transgenic Assay, Control

    Analysis of levels of  minzasolmin  in plasma and brain samples.

    Journal: NPJ Parkinson's Disease

    Article Title: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson’s disease

    doi: 10.1038/s41531-023-00552-7

    Figure Lengend Snippet: Analysis of levels of minzasolmin in plasma and brain samples.

    Article Snippet: Male C57BL/6 mice (8 weeks of age, 20–27 g), purchased from Charles River Laboratories (Toulouse, France), were dosed intraperitoneally with 1 or 5 mg/kg of minzasolmin (10 mL/kg of 40% w/v Captisol® in water).

    Techniques: Clinical Proteomics, Transgenic Assay