ANA-12

N.º de catálogoS7745 Lote:S774501

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Datos técnicos

Fórmula

C22H21N3O3S
Peso molecular 407.49 Número CAS 219766-25-3
Solubilidad (25°C)* In vitro DMSO 37 mg/mL (90.79 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Agregue los solventes al producto individualmente y en orden.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml significa ligeramente soluble o insoluble.
* Tenga en cuenta que Selleck prueba la solubilidad de todos los compuestos internamente, y la solubilidad real puede diferir ligeramente de los valores publicados. Esto es normal y se debe a ligeras variaciones entre lotes.
* Envío a temperatura ambiente (Las pruebas de estabilidad demuestran que este producto se puede enviar sin medidas de refrigeración.)

Preparación de soluciones madre

Actividad biológica

Descripción ANA-12 es un antagonista selectivo de TrkB con una Kd de 10 nM y 12 μM para los sitios de alta y baja afinidad, respectivamente.
Objetivos
TrkB
10 nM(Kd)
In vitro ANA-12 binds directly and selectively to TrkB and inhibits processes downstream of TrkB without altering TrkA and TrkC functions. In nnr5 PC12-TrkB cells, this compound prevents brain-derived neurotrophic factor (BDNF)-induced neurite outgrowth at concentrations as low as 10 nM. In DRG neurons, this chemical eliminates the effect of BDNF on increasing inward current.
In vivo In adult C57BL6/129SveV F1s mice, ANA-12 (0.5 mg/kg, i.p.) decreases TrKB activity in the brain and reduces the anxiety- and depression-related behaviors without affecting the neuron survival. In male C57BL/6 mice, this compound shows antidepressant-like effects on lipopolysaccharide-induced depression-like behavior. In male Sprague-Dawley rats, this chemical blocks the effect of medial nucleus tractus solitarius (mNTS) BDNF on reducing food intake. In male wild-type mice, it reverses ethanol intake and induces D3 receptor downregulation, but is ineffective in D3R-/- mice. In male CocSired rats, this compound reverses the diminished self-administration of cocaine.

Protocolo (de referencia)

Ensayo de quinasa:

[1]
  • ANA-12 Binding assay

    Maxisorp ELISA 96-well plates are coated with various concentrations of Trk BECD -Fc, 20 mg/ml BSA, or 1 mg/mL IgG-Fc (polyclonal anti-TrkB) in a carbonate buffer (pH 9.6) overnight at 4°C. Plates are saturated with 0.5% BSA in PBS for 2 hours at room temperature and extensively washed in PBS-Tween 0.05%. Bodipy–ANA-12 is then incubated in 0.5% PBS-BSA for 1 hour at room temperature before the addition of BDNF in 0.5% PBS-BSA for another hour. After extensive washes in PBS-Tween 0.05%, the amount of bodipy–this compound bound is quantified by fluorescence at 520 ± 10 nm. Detectability range for extrapolation analysis is assessed by coating ELISA plates with bodipy–this chemical and reading fluorescence at 520 ± 10 nm.
Ensayo celular:

[1]
  • Líneas celulares

    nnr5 PC12–TrkA, nnr5 PC12–TrkB, and nnr5 PC12–TrkC cells

  • Concentraciones

    ~100 μM

  • Tiempo de incubación

    ~3 days

  • Método

    Modulation of neurite outgrowth by molecules is assessed in nnr5 PC12–TrkB, –TrkA, and –TrkC cells after addition of BDNF (1 nM), NGF (2 nM), and NT-3 (10 nM), respectively. The number of cells bearing neurites longer than 2 cells in diameter in each counting field is microscopically determined (2 fields per well, 3 wells per condition). Counting is performed blind each 24 hours for 3 days.
Estudio en animales:

[1]
  • Modelos animales

    Adult C57BL6/129SveV F1s mice

  • Dosificaciones

    0.5 mg/kg

  • Administración

    i.p.

Referencias

  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3083767/
  • https://pubmed.ncbi.nlm.nih.gov/24611998/
  • https://pubmed.ncbi.nlm.nih.gov/25628381/
  • https://pubmed.ncbi.nlm.nih.gov/22374757/
  • https://pubmed.ncbi.nlm.nih.gov/24584330/
  • https://pubmed.ncbi.nlm.nih.gov/23242310/

Validación de productos por parte del cliente

Maternal exercise ameliorated sevoflurane-induced neuronal cell loss and decreased dendritic spine density, blocked by TrkB inhibition. Nissl staining and Golgi staining were performed after behavior tests (n = 3). (A) Nissl staining in the CA1 region of hippocampus under ×400. (B) Neuronal density ratio changes. (C) Golgi staining in the CA1 of hippocampus under ×1000. (D) Histograms represented the number of dendritic spines/10 μm. Values are mean ± S.E.M. *p < 0.05, compared with Ctrl group; **p < 0.01, compared with Ctrl group; ##p < 0.01, compared with Sevo group; ∧∧p < 0.01, compared with Sevo + ME group. One-way analysis of variance followed by Tukey post hoc multiple comparison tests was used for data analysis.

Datos de [ , , Front Cell Neurosci, 2018, doi:10.3389/fncel.2018.00122 ]

Total Ca2+/calmodulin-dependent protein kinase II (CaMKII) (pan) and phosphorylated (p-)CaMKII protein expression with representative Western blot images and p-CaMKII-to-CaMKII (pan) ratio in the noninfarct area of the left ventricle (LV) of rats at 5 wk postmyocardial infarction (post-MI) with or without exercise training or ANA-12 treatment. Representative Western blot images of p-CaMKII and CaMKII (pan) with GAPDH as the loading control (A), p-CaMKII (B) and CaMKII (pan) (C) protein expression, and the p-CaMKII-to-CaMKII (pan) ratio in the LV of sham and MI rats with or without exercise training or ANA-12 treatment (D) are shown. Values are means ± SE. Sham group, n = 10; sedentary MI with vehicle treatment (Sed-MI-Veh) group, n = 8; exercise training with MI and vehicle treatment (ExT-MI-Veh) group, n = 9; and exercise training with MI and ANA-12 treatment (ExT-MI-ANA-12) group, n = 8. All bands were normalized to GAPDH and are shown as fold values of the sham group. Statistical analysis was done by one-way ANOVA followed by a Bonferroni post hoc test. For p-CaMKII, F = 6.1, P < 0.01; for CaMKII (pan), F = 1.5, not significant; for p-CaMKII/CaMKII (pan), F = 12.9, P < 0.001. **P < 0.01, and ***P < 0.001 vs. the sham group.

Datos de [ , , Am J Physiol Heart Circ Physiol, 2018, doi:10.1152/ajpheart.00245.2018 ]

(D) when examined on day 11 after stress withdrawal. *p < 0.05 and ***p < 0.001 comparison to vehicle-treated stressed rats, and #p < 0.05 and ###p < 0.001 comparison to apelin-13-treated stressed rats. CWIRS, chronic water-immersion restraint stress; Apelin, apelin-13.

Datos de [ , , Neuroscience, 2018, 390:151-159 ]

Sellecks ANA-12 Ha sido citado por 47 Publicaciones

A Novel Gastrodin Derivative with Neuroprotection Promotes NGF-Mimic Activity by Targeting INSR and ACTN4 to Activate PI3K/Akt Signaling Pathway in PC12 Cells [ Antioxidants (Basel), 2025, 14(3)344] PubMed: 40227445
A novel synthetic 3,4,5-tri-feruloylquinic acid enhances learning and memory via neurotrophin signaling in an aging model senescence-accelerated prone 8 mice [ Geroscience, 2025, 10.1007/s11357-025-01783-7] PubMed: 40699486
ANA-12 Targets and Inhibits BDNF/TrkB Signaling to Alleviate Pain Behaviors in Rheumatoid Arthritis Mice [ Neurochem Res, 2025, 50(4):234] PubMed: 40673956
Neuronal FSTL4 negatively regulates BDNF-mediated neuron-glioma interaction [ Neurochem Int, 2025, 191:106072] PubMed: 41082941
Club cell-derived brain-derived neurotrophic factor regulates murine airway mechanics and mucin production in response to IL-13 in a sex-dependent manner [ Front Physiol, 2025, 16:1578553] PubMed: 40626045
Allium Macrostemon Bge. Attenuates the Cognitive Decline of Aging Mice by Enhancing BDNF/TrkB Pathway [ Food Sci Nutr, 2025, 13(3):e70010] PubMed: 40027296
Isoform-Specific Roles of NTRK2 in Pulmonary Vascular Regeneration [ bioRxiv, 2025, 2025.05.11.653351] PubMed: 40463206
Progressive reduction of nuclear receptor Nr4a1 mediates age-dependent cognitive decline [ Alzheimers Dement, 2024, 10.1002/alz.13819] PubMed: 38605605
HDAC6-dependent deacetylation of NGF dictates its ubiquitination and maintains primordial follicle dormancy [ Theranostics, 2024, 14(6):2345-2366] PubMed: 38646645
A rare olive compound oleacein functions as a TrkB agonist and mitigates neuroinflammation both in vitro and in vivo [ Cell Commun Signal, 2024, 22(1):309] PubMed: 38835076

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