Naloxone-d5
Based on 1 Customer Validation
Naloxone-d5 is the deuterated-labeled Naloxone (HY-17417A). Naloxone is an orally active opioid receptor antagonist. Naloxone attenuates spinal cord stimulation‑associated anti‑hyperalgesic effects, antagonizes physiologic effects of endogenous opioid peptides linked to central nervous system injury sequelae, functions as a pressor agent to induce modest elevations in mean arterial blood pressure, exerts neuroprotective effects to improve post‑traumatic neurologic motor function, blocks opioid receptor‑mediated amnesic pathways, enhances memory consolidation, reverses Adrenocorticotropic hormone (ACTH) (HY-106373)‑ and epinephrine‑induced amnesia, and potentiates the memory‑facilitatory effects of ACTH and epinephrine.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Pureté : 99.60%
- CAS No.: 1261079-38-2
- Formule: C19H16D5NO4
- Masse moléculaire:332.41
-
Stockage:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Voir tous les produits spécifiques à Isoform Opioid Receptor
More
Activité biologique
Description
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
-
CAS No. 1261079-38-2
-
Unlabeled CAS 465-65-6
-
Appearance Solid
-
Masse moléculaire 332.41
-
Formule C19H16D5NO4
-
SMILES
OC1=C(O2)C([C@]([C@]2([H])C(CC3)=O)(CCN4C([2H])([2H])/C([2H])=C([2H])/[2H])[C@]3(O)[C@H]4C5)=C5C=C1
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Protocole
-
Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Pureté et documentation
-
Fiche technique (294 KB)
-
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
-
Instruction de manipulation (2659 KB)
Références
[1]. Sun L, et al. Endocannabinoid activation of CB receptors contributes to long-lasting reversal of neuropathic pain by repetitive spinal cord stimulation. European journal of pain (London, England). 2017 May;21(5):804-814. [Content Brief]
[2].
McIntosh TK, et al. Beneficial effect of the nonselective opiate antagonist naloxone hydrochloride and the thyrotropin-releasing hormone (TRH) analog YM-14673 on long-term neurobehavioral outcome following experimental brain injury in the rat. J Neurotrauma. 1993 Winter;10(4):373-84.
[Content Brief]
[3]. Izquierdo I, et al. Effect of ACTH, epinephrine, beta-endorphin, naloxone, and of the combination of naloxone or beta-endorphin with ACTH or epinephrine on memory consolidation. Psychoneuroendocrinology. 1983;8(1):81-7. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)