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Status:
US Approved Rx
(2024)
Source:
ANDA205147
(2024)
Source URL:
First approved in 2009
Source:
NDA022256
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Dextromilnacipran (1R, 2S/F2696) is an enantiomer of milnacipran, a serotonin/norepinephrine (5-HT/NE) reuptake inhibitor. Dextromilnacipran is pharmacologically less active as compared with racemic mixture and levomilnacipran (1S, 2R/F2695).
Status:
US Approved Rx
(2010)
Source:
NDA022488
(2010)
Source URL:
First approved in 2004
Source:
NDA021723
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pregabalin, marketed under the brand name Lyrica among others. LYRICA is indicated for: Neuropathic pain associated with diabetic peripheral neuropathy (DPN) Postherpetic neuralgia (PHN); Adjunctive therapy for adult patients with partial onset seizures; Fibromyalgia; Neuropathic pain associated with spinal cord injury. It has been shown the clinical effects of pregabalin are likely due to direct and selective interactions with α(2)δ-1 and α(2)δ-2 subunits of voltage-gated calcium channels. 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.
Status:
US Approved Rx
(2010)
Source:
NDA022488
(2010)
Source URL:
First approved in 2004
Source:
NDA021723
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pregabalin, marketed under the brand name Lyrica among others. LYRICA is indicated for: Neuropathic pain associated with diabetic peripheral neuropathy (DPN) Postherpetic neuralgia (PHN); Adjunctive therapy for adult patients with partial onset seizures; Fibromyalgia; Neuropathic pain associated with spinal cord injury. It has been shown the clinical effects of pregabalin are likely due to direct and selective interactions with α(2)δ-1 and α(2)δ-2 subunits of voltage-gated calcium channels. 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.
Status:
US Approved Rx
(2010)
Source:
NDA022488
(2010)
Source URL:
First approved in 2004
Source:
NDA021723
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pregabalin, marketed under the brand name Lyrica among others. LYRICA is indicated for: Neuropathic pain associated with diabetic peripheral neuropathy (DPN) Postherpetic neuralgia (PHN); Adjunctive therapy for adult patients with partial onset seizures; Fibromyalgia; Neuropathic pain associated with spinal cord injury. It has been shown the clinical effects of pregabalin are likely due to direct and selective interactions with α(2)δ-1 and α(2)δ-2 subunits of voltage-gated calcium channels. 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.
Status:
US Approved Rx
(2013)
Source:
ANDA090694
(2013)
Source URL:
First approved in 2004
Source:
NDA021427
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Duloxetine (brand names Cymbalta, Yentreve, and in parts of Europe, Xeristar or Ariclaim) is indicated for the acute and maintenance treatment of major depressive disorder (MDD), as well as acute management of generalized anxiety disorder. Also used for the management of neuropathic pain associated with diabetic peripheral neuropathy, and fibromyalgia. Has been used in the management of moderate to severe stress urinary incontinence (SUI) in women. It is manufactured and marketed by Eli Lilly and Company. Duloxetine has not yet been FDA approved for stress urinary incontinence or for fibromyalgia. Duloxetine is a selective SNRI (selective serotonin-norepinephrine reuptake inhibitor). Duloxetine is a systemic drug therapy which affects the body as a whole. Known also under the code name LY248686, it is a potent dual reuptake inhibitor of serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine (NE), possessing comparable affinities in binding to NE- and 5-HT transporter sites. It is a less potent inhibitor of dopamine reuptake.
Status:
US Approved OTC
Source:
21 CFR 331.11(g)(6) antacid:magnesium-containing magnesium hydroxide
Source URL:
First marketed in 1921
Source:
Solution of Magnesium Citrate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.
Status:
US Approved OTC
Source:
21 CFR 331.11(g)(6) antacid:magnesium-containing magnesium hydroxide
Source URL:
First marketed in 1921
Source:
Solution of Magnesium Citrate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.
Status:
US Approved OTC
Source:
21 CFR 331.11(g)(6) antacid:magnesium-containing magnesium hydroxide
Source URL:
First marketed in 1921
Source:
Solution of Magnesium Citrate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.
Status:
US Approved OTC
Source:
21 CFR 331.11(g)(6) antacid:magnesium-containing magnesium hydroxide
Source URL:
First marketed in 1921
Source:
Solution of Magnesium Citrate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.
Status:
US Approved OTC
Source:
21 CFR 331.11(g)(6) antacid:magnesium-containing magnesium hydroxide
Source URL:
First marketed in 1921
Source:
Solution of Magnesium Citrate U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.