| Identification | Back Directory | [Name]
7H-Purine-7-acetamide, 1,2,3,6-tetrahydro-1,3-dimethyl-N-(1-methylethyl)-N-[[(1-methylethyl)amino]carbonyl]-2,6-dioxo- | [CAS]
1372206-64-8 | [Synonyms]
1,2,3,6-tetrahydro-1,3-dimethyl-N-(1-methylethyl)-N-[[(1-methylethyl)amino]carbonyl]-2,6-dioxo-7H-Purine-7-acetamide
7H-Purine-7-acetamide, 1,2,3,6-tetrahydro-1,3-dimethyl-N-(1-methylethyl)-N-[[(1-methylethyl)amino]carbonyl]-2,6-dioxo- | [Molecular Formula]
C16 H24 N6 O4 | [MOL File]
1372206-64-8.mol | [Molecular Weight]
364.4 |
| Chemical Properties | Back Directory | [density ]
1.35±0.1 g/cm3(Predicted) | [storage temp. ]
4°C, protect from light | [solubility ]
DMSO : 100 mg/mL (274.42 mM; Need ultrasonic) | [form ]
Solid | [pka]
12.56±0.46(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
THX-B is a potent and non-peptidic p75NTR (neurotrophin receptor p75) antagonist. THX-B can be used in the research of diabetic kidney disease, neurodegenerative and inflammatory disorders[1][2][3]. | [in vivo]
THX-B (50 μg in 125 μL PBS, i.p. weekly for 4 weeks) improves bladder function in a mouse model of diabetic voiding dysfunction[3].
THX-B (2?μL of 2?μg/μL, IVT injection, a single dose) elicits a neuroprotective effect on photoreceptor cells in P17 rd10 mice[2].
THX-B (40 μg in 20 μL, IVT injection) resolves the inflammatory, vascular, and neurodegenerative phases of the retinal pathology[4].
| Animal Model: | Mouse model of diabetic voiding dysfunction | | Dosage: | 50 μg in 125 μL PBS | | Administration: | Intraperitoneal injection (i.p.) | | Result: | Prevented bladder weight increase, which was 18% (95% CI 3%, 32%) and 37% (95% CI 14%, 60%) lower after 2 and 4 weeks of treatment.
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| Animal Model: | P17 rd10 mice[1] | | Dosage: | 2?μL of 2?μg/μL, single dose | | Administration: | Intravitreal (IVT) injected in one eye | | Result: | Increased the number of photoreceptor rows as well as the ONL/INL ratio.
Decreased the total number of microglial cells in the treated retinas, as well as some of the inflammatory signs, such as GFAP, α2M and the proinflammatory cytokines IL-1β and TNFα.
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| [References]
[1] Keren Ettinger, et al. Nerve growth factor stimulation of ERK1/2 phosphorylation requires both p75NTR and α9β1 integrin and confers myoprotection towards ischemia in C2C12 skeletal muscle cell model. Cell Signal. 2012 Dec;24(12):2378-88. DOI:10.1016/j.cellsig.2012.08.008
[2] María Platón-Corchado, et al. p75NTR antagonists attenuate photoreceptor cell loss in murine models of retinitis pigmentosa. Cell Death Dis. 2017 Jul 13;8(7):e2922. DOI:10.1038/cddis.2017.306
[3] Abubakr H Mossa, et al. Antagonism of proNGF or its receptor p75 NTR reverses remodelling and improves bladder function in a mouse model of diabetic voiding dysfunction. Diabetologia. 2020 Sep;63(9):1932-1946. DOI:10.1007/s00125-020-05222-4
[4] Alba Galan, et al. Subconjunctival Delivery of p75NTR Antagonists Reduces the Inflammatory, Vascular, and Neurodegenerative Pathologies of Diabetic Retinopathy. Invest Ophthalmol Vis Sci. 2017 Jun 1;58(7):2852-2862. DOI:10.1167/iovs.16-20988 |
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