Pregabalin Powder CAS: 148553-50-8 Pharmaceutical Raw Materials
|FOB Price:||US $0.5 / ml|
|Min. Order:||100 ml|
|Min. Order||FOB Price|
|100 ml||US $0.5/ ml|
|Transport Package:||Bottle or Drum|
|Payment Terms:||T/T, Western Union, Paypal, Money Gram, Bitcoin|
- Model NO.: 148553-50-8
- Customized: Non-Customized
- State: Powder
- MOQ: 100ml
- Appearance: White Powder
- Molecular Formula: C8h17no2
- CAS: 148553-50-8
- Specification: USP/EP/BP
- HS Code: 3402
- Powder: Yes
- Certification: GMP, ISO 9001, USP
- Purity: >99%
- Product Name: Pregabalin
- Assay: 99%
- Capacity: 2000kg
- Trademark: Yijing
- Origin: Shanghai, China
Pregabalin is ananticonvulsant drug used for neuropathic pain and as an adjunct therapy for partial seizures with or without secondary generalization in adults. It has also been found effective for generalized anxiety disorder and is (as of 2007) approved for this use in the European Union. It was designed as a more potent successor to gabapentin. Pregabalin is marketed byunder the trade name Lyrica. described in an SEC filing that the drug could be used to treat epilepsy, post-herpetic neuralgia and diabetic peripheral neuropathy, fibromyalgia, et al. Sales reached a record $3.063 billion in 2010.
Recent studies have shown that pregabalin is effective at treating chronic pain in disorders such as fibromyalgia and spinal cord injury. In June 2007, pregabalin became the first medication approved by the U.S.Food and Drug Administration specifically for the treatment offibromyalgia.
It is considered to have a low potential for abuse, and a limited dependence liability if misused, and is thus classified as a Schedule Vdrug in the U.S.
Lyrica is one of four drugs which a subsidiary of in 2009 pleaded guilty to misbranding "with the intent to defraud or mislead". agreed to pay $2.3 billion (£1.4 billion) in settlement, and entered a corporate integrity agreement.illegally promoted the drugs and caused false claims to be submitted to government healthcare programs for uses that were not approved by the U.S. Food and Drug Administration(FDA).
Pregabalin is available in 25, 50, 75, 100, 150, 200, 225, and 300 mg capsules, and recently a strawberry-flavoured oral solution has been developed, containing 20 mg/mL with an added sweetening agent (sucrose) to mask the chemical's bitter taste. The maximum daily recommended dose for pregabalin is 600 mg. Dosages must be monitored and increases should be based on patient's tolerance.
Pregabalin is used for the management of neuropathic pain associated with diabetic peripheral neuropathy or spinal cord injury, and postherpetic neuralgia. It is also used as adjunctive therapy for adult patients with partial onset seizures and management of fibromyalgia.
Pregabalin is a new anticonvulsant drug indicated as an add on therapy for partial onset seizures and for certain types of neuropathic pain. It was designed as a more potent successor to a related drug, gabapentin. Pregabalin binds to the alpha2-delta subunit of the voltage-gated calcium channel in the central nervous system. While pregabalin is a structural derivative of the inhibitory neurotransmitter gamma- aminobutyric acid (GABA), it does not bind directly to GABAA, GABAB, or benzodiazepine receptors, does not augment GABAA responses in cultured neurons, does not alter rat brain GABA concentration or have acute effects on GABA uptake or degradation. However, in cultured neurons prolonged application of pregabalin increases the density of GABA transporter protein and increases the rate of functional GABA transport. Pregabalin does not block sodium channels, is not active at opiate receptors, and does not alter cyclooxygenase enzyme activity. It is inactive at serotonin and dopamine receptors and does not inhibit dopamine, serotonin, or noradrenaline reuptake.
Mechanism of action
Pregabalin binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues. Although the mechanism of action of pregabalin is unknown, results with genetically modified mice and with compounds structurally related to pregabalin (such as gabapentin) suggest that binding to the alpha2-delta subunit may be involved in pregabalin's antinociceptive and antiseizure effects in animal models. In vitro, pregabalin reduces the calcium-dependent release of several neurotransmitters, possibly by modulation of calcium channel function. Studies also suggest that the descending noradrenergic and serotonergic pathways originating from the brainstem may be involved with the mechanism of pregabalin. Interestingly, although pregabalin is a structural derivative of inhibitory neurotransmitter gamma-aminobutyric acid (GABA), it does not bind directly to GABA or benzodiazepine receptors. The sodium channels, opiate receptors, and cyclooxygenase enzymes are not involved with the mechanism of pregabalin. It is also inactive at serotonin and dopamine receptors and does not inhibit dopamine, serotonin, or noradrenaline reuptake.
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