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Sufentanil Powder is an Opioid Agonist. The system of activity of sufentanil is as a Full Opioid Agonist. Sufentanil is a narcotic pain relieving that is utilized as an extra in sedation, in adjusted sedation, and as an essential sedative specialist. It is regulated by the intravenous, epidural and sublingual courses.

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Sufentanil Powder is a potent opioid agonist utilized as an adjunct in anesthesia, in balanced sedation, and as a primary sedative agent. It is administered intravenously, epidurally, and sublingually. Also known as Dsuvia, its sublingual form is indicated for managing severe acute pain in adults in medically supervised healthcare settings, including hospitals, surgical centers, and emergency departments. Potential military applications for immediate pain relief may also be considered in the future.

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**IUPAC Name:** N-[4-(methoxymethyl)- 1-(2-thiophen-2-ylethyl)piperidin-4-yl]-N-phenylpropanamide

**InChI:** InChI=1S/C22H30N2O2S/c1-3-21(25)24(19-8-5-4-6-9-19)22(18-26-2)12-15-23(16-13-22)14-11-20-10-7-17-27-20/h4-10,17H,3,11-16,18H2,1-2H3

**InChI Key:** GGCSSNBKKAUURC-UHFFFAOYSA-N

**Standard SMILES:** CCC(=O)N(C1=CC=CC=C1)C2(CCN(CC2)CCC3=CC=CS3)COC

**Atomic Formula:** C22H30N2O2S

**Medication Indication**

Sufentanil is used as follows:

1. Adjunct to maintain balanced general sedation in intubated and ventilated patients.
2. Primary sedative for induction and maintenance of anesthesia in major surgeries, especially in cardiovascular or neurosurgical procedures.
3. Epidurally for analgesia during labor and vaginal delivery.
4. Sublingually for managing severe acute pain in adults in medically supervised healthcare settings.

**Mechanism of Action**

Sufentanil is a synthetic opioid that binds highly selectively to µ-opioid receptors, distributed throughout the human brain, spinal cord, and other tissues. Its actions include reducing cAMP levels, inhibiting neurotransmitter release, and causing membrane hyperpolarization, all contributing to pain relief. It modulates synaptic neural transmission and opens calcium-dependent inwardly rectifying potassium channels, resulting in neuronal hyperpolarization and reduced sensitivity.

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