5-Thiazolecarboxamide, N-[(1R)-1-(1H-indol-3-ylmethyl)pentyl]-2-(4-methyl-1-piperazinyl)- manufacturers
- Minzasolmin
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- $245.00
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2026-07-15
- CAS:1802518-92-8
- Purity: 99.95%
- Supply Ability: 10g
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| | 5-Thiazolecarboxamide, N-[(1R)-1-(1H-indol-3-ylmethyl)pentyl]-2-(4-methyl-1-piperazinyl)- Basic information |
| | 5-Thiazolecarboxamide, N-[(1R)-1-(1H-indol-3-ylmethyl)pentyl]-2-(4-methyl-1-piperazinyl)- Chemical Properties |
| density | 1.209±0.06 g/cm3(Predicted) | | pka | 13.93±0.46(Predicted) | | form | Solid | | color | Off-white to light yellow |
| | 5-Thiazolecarboxamide, N-[(1R)-1-(1H-indol-3-ylmethyl)pentyl]-2-(4-methyl-1-piperazinyl)- Usage And Synthesis |
| Uses | Minzasolmin (NPT200-11; UCB0599) is an orally active, blood-brain-permeable α-synuclein (α-Syn) inhibitor that selectively binds to α-Syn misfolded intermediates (such as oligomers) and inhibits aggregation and fibril formation by regulating their conformational stability. Minzasolmin can reduce the generation of pathological oligomers and block neurotoxic signaling, thereby reducing the abnormal accumulation of α-Syn in the brain. Minzasolmin significantly improved motor deficits, reduced neuroinflammatory markers, and α-Syn-related pathological deposition in transgenic mouse models[1][2]. | | in vivo | Minzasolmin (1 mg/kg, 5 mg/kg; intraperitoneal injection; once a day, 5 days a week; 3 months) significantly improves motor coordination ability (such as prolonged rotarod test time), reduces α-synuclein (α-Syn) pathological deposition and neuroinflammatory markers (such as reduced IL-6 levels) in the cerebral cortex and hippocampus, and restores striatal dopamine transporter (DAT) levels in the Thy1-αSyn transgenic mouse model[1]. | Animal Model: | Female Thy1-αSyn transgenic mice[2] | | Dosage: | 1 mg/kg or 5 mg/kg, dissolved in DMSO/saline | | Administration: | Intraperitoneal (IP) injection, daily (Monday to Friday), 3-month treatment period | | Result: |
Significantly improved motor coordination (rotarod latency increased by 20% in 5 mg/kg group) and reduced gait abnormalities compared to vehicle controls.
Western blot analysis showed a dose-dependent decrease in insoluble α-synuclein (α-Syn) aggregates in the cortex and hippocampus (50% reduction at 5 mg/kg), accompanied by downregulation of neuroinflammatory markers (IL-6, TNF-α) and normalization of striatal dopamine transporter (DAT) levels.
Immunohistochemistry revealed fewer phosphorylated α-Syn (p-Ser129) positive inclusions in substantia nigra neurons, indicating attenuation of α-Syn pathology and neuroinflammation. |
| | IC 50 | α-synuclein Aggregation | | References | [1] Steiner MA. Matters arising: In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson's disease. NPJ Parkinsons Dis. 2024 Mar 14;10(1):59. DOI:10.1038/s41531-024-00657-7
[2] Baggett, et al. Novel Approaches Targeting in α-Synuclein for Parkinson's Disease: Current Progress and Future Directions for the Disease-Modifying Therapies. Brain Disorders (2024): 100163. |
| | 5-Thiazolecarboxamide, N-[(1R)-1-(1H-indol-3-ylmethyl)pentyl]-2-(4-methyl-1-piperazinyl)- Preparation Products And Raw materials |
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