D0V6OZ |
CN-105 |
Unclearntraumatic intracerebral hemorrhage |
Phase 2 |
APOE |
APOE |
Agonist |
Here using human iPSC-derived cerebral organoid models, we find that APOE deletion increases alpha-synuclein (alphaSyn) accumulation accompanied with synaptic loss, reduction of GBA levels, lipid droplet accumulation and dysregulation of intracellular organelles. |
-8.28 |
more |
D03SHD |
Myo-inositol |
Alzheimer disease |
Phase 2 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D06KWU |
DWP-09031 |
Alzheimer disease |
Phase 1 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D07VAI |
ALZ-801 |
Alzheimer disease |
Phase 2 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D08QDF |
Systebryl |
Amyloidosis |
Phase 1 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D09DLP |
Tramiprosate |
Alzheimer disease |
Phase 3 |
APP |
APP |
Antagonist |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D0CH6B |
ALZT-OP1 |
Alzheimer disease |
Phase 3 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D0E8HA |
T-817MA |
Alzheimer disease |
Phase 2 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D0G7LP |
Pepticlere |
Alzheimer disease |
Preclinical |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D0W0NU |
NIC5-15 |
Alzheimer disease |
Phase 2 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D0X4ZL |
AN-1792 |
Alzheimer disease |
Phase 2 |
APP |
APP |
Inhibitor |
The 5XFAD model over-express human amyloid precursor protein (APP) and presenilin 1 (PS1) harboring five familial AD mutations, which have a high APP expression correlating with a high burden and an accelerated accumulation of the 42 amino acid species of amyloid-beta. |
-8.09 |
more |
D01EJG |
RG6100 |
Alzheimer disease |
Phase 2 |
MAPT |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-8.00 |
more |
D0I3LY |
PMID28766366-Compound-Scheme22Middle |
Unclear |
Patented |
MAPT |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-8.00 |
more |
D0I8FS |
BIIB092 |
Progressive supranuclear palsy | Alzheimer disease |
Phase 2 |
MAPT |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-8.00 |
more |
D0P8YJ |
PTI-80 |
Alzheimer disease |
Phase 1 |
MAPT |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-8.00 |
more |
D5FSV8 |
TRx0237 |
Alzheimer disease |
Phase 3 |
MAPT |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-8.00 |
more |
D05XDZ |
LMT-X |
Acute myeloid leukaemia | Alzheimer disease |
Phase 3 |
MAPT/TARDBP |
TARDBP |
Inhibitor |
Additionally, in Drosophila models of ALS and human neuronal cells, scientists found that overexpression of TAR DNA-binding protein 43 (TDP-43) can inhibit HSPA8 transcription, leading to the dysfunction of synaptic vesicle cycling all of which is associated with microautophagy dysfunction. |
-6.46 |
more |
D05XDZ |
LMT-X |
Acute myeloid leukaemia | Alzheimer disease |
Phase 3 |
MAPT/TARDBP |
MAPT |
Inhibitor |
Since gain-of-function mutations of the MAPT gene cause frontotemporal lobar degeneration (FTLD) characterized by deposition of tau protein, we hypothesize that MAPT duplication affecting gene dosage could also lead to disease. |
-6.46 |
more |
D01LOE |
LY2963016 |
Type-1/2 diabetes |
Phase 3 |
INS |
INS |
Agonist |
Results: CNN-derived image phenotypes are significantly associated with fasting metabolites related to early lipid metabolic changes as well as insulin resistance and with genetic variants mapped to candidate genes enriched for amyloid beta degradation, tau phosphorylation, calcium ion binding-dependent synaptic loss, APP-regulated inflammation response, and insulin resistance. |
-5.50 |
more |
D01UYA |
MEDI1341 |
Parkinson disease |
Phase 1 |
SNCA |
SNCA |
Inhibitor |
We show here, in the MPP+ (1-methyl-4-phenylpyridinium ion) cell model of parkinsonism, a time- and dose-dependent increase in the hyperphosphorylation of Tau at pSer396/404 (PHF-1-reactive Tau, p-Tau), concomitant with increased accumulation of alpha-Syn, upon treatment of cells with the neurotoxin. |
-5.08 |
more |
D0TU9W |
BIIB054 |
Parkinson disease |
Phase 2 |
SNCA |
SNCA |
Inhibitor |
We show here, in the MPP+ (1-methyl-4-phenylpyridinium ion) cell model of parkinsonism, a time- and dose-dependent increase in the hyperphosphorylation of Tau at pSer396/404 (PHF-1-reactive Tau, p-Tau), concomitant with increased accumulation of alpha-Syn, upon treatment of cells with the neurotoxin. |
-5.08 |
more |
D4N2JV |
PRX002 |
Parkinson disease |
Phase 2 |
SNCA |
SNCA |
Inhibitor |
We show here, in the MPP+ (1-methyl-4-phenylpyridinium ion) cell model of parkinsonism, a time- and dose-dependent increase in the hyperphosphorylation of Tau at pSer396/404 (PHF-1-reactive Tau, p-Tau), concomitant with increased accumulation of alpha-Syn, upon treatment of cells with the neurotoxin. |
-5.08 |
more |
DIW37N |
NPT200-11 |
Multiple system atrophy | Parkinson disease |
Phase 1 |
SNCA |
SNCA |
Inhibitor |
We show here, in the MPP+ (1-methyl-4-phenylpyridinium ion) cell model of parkinsonism, a time- and dose-dependent increase in the hyperphosphorylation of Tau at pSer396/404 (PHF-1-reactive Tau, p-Tau), concomitant with increased accumulation of alpha-Syn, upon treatment of cells with the neurotoxin. |
-5.08 |
more |
D06WPM |
Coprexa |
Neurological disorder |
Phase 3 |
SOD1 |
SOD1 |
Inhibitor |
KEY FINDINGS: The results showed that apoptosis and reactive oxygen species levels significantly increased in Abeta25-35-treated cells, whereas the mRNA and protein levels of Nrf2, SOD and HO-1 decreased. |
-5.06 |
more |
D0D9NZ |
Methoxyestradiol |
Unclear |
Phase 2 |
SOD1 |
SOD1 |
Inhibitor |
KEY FINDINGS: The results showed that apoptosis and reactive oxygen species levels significantly increased in Abeta25-35-treated cells, whereas the mRNA and protein levels of Nrf2, SOD and HO-1 decreased. |
-5.06 |
more |
D0I1CQ |
BIIB067 |
Amyotrophic lateral sclerosis |
Phase 3 |
SOD1 |
SOD1 |
Inhibitor |
KEY FINDINGS: The results showed that apoptosis and reactive oxygen species levels significantly increased in Abeta25-35-treated cells, whereas the mRNA and protein levels of Nrf2, SOD and HO-1 decreased. |
-5.06 |
more |
D0T8MA |
ATN-224 |
Solid tumour/cancer |
Phase 2 |
SOD1 |
SOD1 |
Inhibitor |
KEY FINDINGS: The results showed that apoptosis and reactive oxygen species levels significantly increased in Abeta25-35-treated cells, whereas the mRNA and protein levels of Nrf2, SOD and HO-1 decreased. |
-5.06 |
more |
D09AYM |
MABp1 |
Colorectal cancer | Type-2 diabetes | Acne vulgaris | Atopic dermatitis | Hidradenitis suppurativa | Plaque psoriasis | Pyoderma gangreUnclearsum | Peripheral vascular disease |
Phase 3 |
IL1A |
IL1A |
Inhibitor |
Subsequently, we exposed NGC0211 cells directly to AD-related factors like amyloid-beta peptides (Abeta40/42) or activated astrocyte-conditioned medium (Abeta40/42/IL-1beta/TNFalpha-treated) and evaluated biochemical stress markers, cell death indicators, cell proliferation marker (Ki67), and hmNGF release. |
-4.51 |
more |
D0I9XH |
Celastrol |
Motor neurone disease |
Preclinical |
TNF/IL1B |
TNF |
Suppressor |
Subsequently, we exposed NGC0211 cells directly to AD-related factors like amyloid-beta peptides (Abeta40/42) or activated astrocyte-conditioned medium (Abeta40/42/IL-1beta/TNFalpha-treated) and evaluated biochemical stress markers, cell death indicators, cell proliferation marker (Ki67), and hmNGF release. |
-4.25 |
more |
D0I9XH |
Celastrol |
Motor neurone disease |
Preclinical |
TNF/IL1B |
IL1B |
Suppressor |
In oxidatively-stressed neural cells and rodents' brains, cytosolic oxidatively-damaged mitochondrial DNA accumulated and increased antiviral and inflammatory proteins, including cleaved caspase-1, interleukin-1beta, and interferon-beta. |
-4.25 |
more |
D0F7DS |
PMID26161698-Compound-18 |
Unclear |
Patented |
GSK3B/CDK5 |
GSK3B |
Inhibitor |
We further showed that miR-219-5p could mediate a decrease in the protein levels of tau-tubulin kinase 1 (TTBK1) and glycogen synthase kinase 3beta (GSK-3beta) by directly binding to their 3'-untranslated region, thereby promoting the phosphorylation of tau in SH-SY5Y Cells. |
-4.03 |
more |
D0F7DS |
PMID26161698-Compound-18 |
Unclear |
Patented |
GSK3B/CDK5 |
CDK5 |
Inhibitor |
Inhibition of miR-132 in primary human neurons and neural cells leads to increased NOS1 levels and triggers excessive production of nitric oxide, followed by aberrant S-nitrosylation (SNO) of specific proteins associated with neurodegeneration and tau pathology, such as cyclin-dependent kinase 5, dynamin-related protein 1, and glyceraldehyde-3-phosphate dehydrogenase. |
-4.03 |
more |
D00EHX |
TT-301 |
Alzheimer disease |
Phase 1 |
IL1B |
IL1B |
Inhibitor |
In oxidatively-stressed neural cells and rodents' brains, cytosolic oxidatively-damaged mitochondrial DNA accumulated and increased antiviral and inflammatory proteins, including cleaved caspase-1, interleukin-1beta, and interferon-beta. |
-4.03 |
more |
D07NSU |
Glucosamine |
Osteoarthritis |
Approved |
IL1B |
IL1B |
Inhibitor |
In oxidatively-stressed neural cells and rodents' brains, cytosolic oxidatively-damaged mitochondrial DNA accumulated and increased antiviral and inflammatory proteins, including cleaved caspase-1, interleukin-1beta, and interferon-beta. |
-4.03 |
more |
D0N1FS |
Diacerein |
Unclear |
Phase 4 |
IL1B |
IL1B |
Inhibitor |
In oxidatively-stressed neural cells and rodents' brains, cytosolic oxidatively-damaged mitochondrial DNA accumulated and increased antiviral and inflammatory proteins, including cleaved caspase-1, interleukin-1beta, and interferon-beta. |
-4.03 |
more |
D0R4ZT |
Gallium nitrate |
Hypercalcaemia |
Approved |
IL1B |
IL1B |
Inhibitor |
In oxidatively-stressed neural cells and rodents' brains, cytosolic oxidatively-damaged mitochondrial DNA accumulated and increased antiviral and inflammatory proteins, including cleaved caspase-1, interleukin-1beta, and interferon-beta. |
-4.03 |
more |
D03DPZ |
INK128 |
Breast cancer | Multiple myeloma |
Phase 2 |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |
D03FCF |
Novolimus |
Artery steUnclearsis |
Approved |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |
D03LJR |
Sirolimus |
Organ transplant rejection | Multiple myeloma | Dutch elm disease |
Approved |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |
D08PSC |
BI 860585 |
Solid tumour/cancer |
Phase 1 |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |
D0ES1Q |
Temsirolimus |
Renal cell carciUnclearma |
Approved |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |
D0H7XL |
OSI-027 |
Renal cell carciUnclearma |
Phase 2 |
MTOR |
MTOR |
Inhibitor |
Specifically, we found that autophagy inhibition increases the accumulation of the C-terminal fragments of TDP-43, whereas inhibition of mTOR, a key protein kinase involved in autophagy regulation, reduces the 25-kDa C-terminal fragment accumulation and restores TDP-43 localization. |
-3.91 |
more |