timapiprant  (MedChemExpress)


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    MedChemExpress timapiprant
    Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as <t>timapiprant,</t> could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .
    Timapiprant, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/timapiprant/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    timapiprant - by Bioz Stars, 2022-05
    94/100 stars

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    1) Product Images from "Prostaglandin D2 pathway in a transgenic rat model of Alzheimer’s disease: therapeutic potential of timapiprant a DP2 antagonist"

    Article Title: Prostaglandin D2 pathway in a transgenic rat model of Alzheimer’s disease: therapeutic potential of timapiprant a DP2 antagonist

    Journal: bioRxiv

    doi: 10.1101/2022.03.30.486444

    Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as timapiprant, could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .
    Figure Legend Snippet: Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as timapiprant, could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .

    Techniques Used: Inhibition, Expressing, Activity Assay

    Timapiprant mitigates AD pathology. Tg-AD timapiprant-treated (TGTR, n = 9) compared to Tg-AD nontreated (TGNT, n = 9) male rats perform significantly better in latency to first entrance during training ( a , p = 0.002) with a significant post-hoc difference on trial 5, experience lower plaque burden ( b , p = 0.001), higher neuronal levels ( c , p = 0.01), and lower microglia levels ( d , p
    Figure Legend Snippet: Timapiprant mitigates AD pathology. Tg-AD timapiprant-treated (TGTR, n = 9) compared to Tg-AD nontreated (TGNT, n = 9) male rats perform significantly better in latency to first entrance during training ( a , p = 0.002) with a significant post-hoc difference on trial 5, experience lower plaque burden ( b , p = 0.001), higher neuronal levels ( c , p = 0.01), and lower microglia levels ( d , p

    Techniques Used:

    Schematic representation of the experimental design a Time line of the progression of the AD pathology developed by Tg-AD rats. b Rat groups used in the study. c Assessments of the AD pathology developed by the Tg-AD rats at 11 months of age. d Timapiprant treatment overview.
    Figure Legend Snippet: Schematic representation of the experimental design a Time line of the progression of the AD pathology developed by Tg-AD rats. b Rat groups used in the study. c Assessments of the AD pathology developed by the Tg-AD rats at 11 months of age. d Timapiprant treatment overview.

    Techniques Used:

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    MedChemExpress timapiprant
    Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as <t>timapiprant,</t> could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .
    Timapiprant, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/timapiprant/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    timapiprant - by Bioz Stars, 2022-05
    94/100 stars
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    Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as timapiprant, could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .

    Journal: bioRxiv

    Article Title: Prostaglandin D2 pathway in a transgenic rat model of Alzheimer’s disease: therapeutic potential of timapiprant a DP2 antagonist

    doi: 10.1101/2022.03.30.486444

    Figure Lengend Snippet: Scheme depicting the relevance of the PGD2 pathway to AD and its potential as a novel multitarget therapeutic for AD Tg-AD rats at 11 months of age exhibited a microglia shift in the hippocampus, from a neuroprotective state typical of ramified microglia to more of a neurotoxic and overactive state attributable to amoeboid microglia. DP1/microglia co-localization at the hippocampal hilar subregion followed the same pattern, increasing the most in amoeboid microglia. Tg-AD rats also displayed DP2 and neuronal losses in the hippocampus. In the brains of AD patients, L-PGDS, the major PGD2 synthase in the brain, is upregulated and Sox-2, a transcription factor, is downregulated. We propose that manipulating PGD2 signaling through, for example DP2 receptor antagonists such as timapiprant, could prevent/mitigate AD neuropathology. DP1 agonists via cAMP convert microglia to a tissue reparative phenotype, protect the brain from ischemic stroke by facilitating vasodilation, and promote sleep that drives Aβ clearance. DP1 antagonists protect against hemorrhagic stroke by limiting bleeding, and mitigate neurotoxic microglia levels. DP2 antagonists prevent neuronal loss, act as antidepressants and improve cognition, potentially via inhibition of the PI3K/AKT/mTOR pathway. L-PGDS, the major PGD2 synthase in the brain, also acts as an Aβ chaperone, inhibits Aβ40/42 aggregation, functions as a disaggregase by disassembling Aβ fibrils, and modulates the expression of Sox-2, a transcription factor. Sox-2 protects against AD neuropathology by interacting with APP and promoting α-secretase activity. Further details are presented in the discussion, based on our current results with the Tg-AD rat model and studies published by others. Figure partially created with BioRender.com .

    Article Snippet: At seven months, Tg-AD and WT rats began timapiprant treatment (cat # HY-15342, MCE, Monmouth Junction, NJ) with 10 mg/kg body weight/day/rat administered orally in rodent chow (Research Diets Inc. NJ) for 4 months.

    Techniques: Inhibition, Expressing, Activity Assay

    Timapiprant mitigates AD pathology. Tg-AD timapiprant-treated (TGTR, n = 9) compared to Tg-AD nontreated (TGNT, n = 9) male rats perform significantly better in latency to first entrance during training ( a , p = 0.002) with a significant post-hoc difference on trial 5, experience lower plaque burden ( b , p = 0.001), higher neuronal levels ( c , p = 0.01), and lower microglia levels ( d , p

    Journal: bioRxiv

    Article Title: Prostaglandin D2 pathway in a transgenic rat model of Alzheimer’s disease: therapeutic potential of timapiprant a DP2 antagonist

    doi: 10.1101/2022.03.30.486444

    Figure Lengend Snippet: Timapiprant mitigates AD pathology. Tg-AD timapiprant-treated (TGTR, n = 9) compared to Tg-AD nontreated (TGNT, n = 9) male rats perform significantly better in latency to first entrance during training ( a , p = 0.002) with a significant post-hoc difference on trial 5, experience lower plaque burden ( b , p = 0.001), higher neuronal levels ( c , p = 0.01), and lower microglia levels ( d , p

    Article Snippet: At seven months, Tg-AD and WT rats began timapiprant treatment (cat # HY-15342, MCE, Monmouth Junction, NJ) with 10 mg/kg body weight/day/rat administered orally in rodent chow (Research Diets Inc. NJ) for 4 months.

    Techniques:

    Schematic representation of the experimental design a Time line of the progression of the AD pathology developed by Tg-AD rats. b Rat groups used in the study. c Assessments of the AD pathology developed by the Tg-AD rats at 11 months of age. d Timapiprant treatment overview.

    Journal: bioRxiv

    Article Title: Prostaglandin D2 pathway in a transgenic rat model of Alzheimer’s disease: therapeutic potential of timapiprant a DP2 antagonist

    doi: 10.1101/2022.03.30.486444

    Figure Lengend Snippet: Schematic representation of the experimental design a Time line of the progression of the AD pathology developed by Tg-AD rats. b Rat groups used in the study. c Assessments of the AD pathology developed by the Tg-AD rats at 11 months of age. d Timapiprant treatment overview.

    Article Snippet: At seven months, Tg-AD and WT rats began timapiprant treatment (cat # HY-15342, MCE, Monmouth Junction, NJ) with 10 mg/kg body weight/day/rat administered orally in rodent chow (Research Diets Inc. NJ) for 4 months.

    Techniques: