Products & Portfolio (14)
1 discontinued product not shown
AMOXICILLIN AND CLAVULANATE POTASSIUM
amoxicillin and clavulanate potassium
Post-LOE
ORAL · FOR SUSPENSION
drugs. [see Microbiology ]
the following infections in adultsskin structure infections Urinary tract infections Limitations of Useindicating no beta-lactamase production+10 more
2023
30
AMOXICILLIN AND CLAVULANATE POTASSIUM
amoxicillin and clavulanate potassium
Post-LOE
ORAL · FOR SUSPENSION
[see Microbiology ( )].
equal to 40 kg with: Recurrentpersistent acute otitis media due to Sacute otitis media due to S+4 more
2023
30
AMOXICILLIN AND CLAVULANATE POTASSIUM
amoxicillin and clavulanate potassium
Post-LOE
ORAL · TABLET
[see Microbiology ()].
the following infections in adultsskin structure infections Urinary tract infections Limitations of Useindicating no beta-lactamase production+10 more
2023
30
AMOXICILLIN AND CLAVULANATE POTASSIUM
amoxicillin and clavulanate potassium
Post-LOE
ORAL · TABLET
[see Microbiology ()].
the following infections in adultsskin structure infections Urinary tract infections Limitations of Useindicating no beta-lactamase production+10 more
2023
30
AMOXICILLIN AND CLAVULANATE POTASSIUM
amoxicillin and clavulanate potassium
Post-LOE
ORAL · FOR SUSPENSION
drug. [see Microbiology ]
the following infections in adultsskin structure infections Urinary tract infections Limitations of Useindicating no beta-lactamase production+10 more
2023
30
CYCLOSPORINE
cyclosporine
Post-LOE
OPHTHALMIC · EMULSION
Calcineurin Inhibitors
2024
30
ESOMEPRAZOLE SODIUM
esomeprazole sodium
Post-LOE
INTRAVENOUS · INJECTABLE
compounds, the substituted benzimidazoles, that suppress gastric acid secretion by specific inhibition of the H/KATPase enzyme system at the secretory surface of the gastric parietal cell. Esomeprazole is protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, esomeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus.
2017
30
FORMOTEROL FUMARATE
formoterol fumarate dihydrate
Post-LOE
INHALATION · SOLUTION
long-acting, beta 2 -adrenergic receptor agonist (beta 2 -agonist). Inhaled formoterol fumarate acts locally in the lung as a bronchodilator. In vitro studies have shown that formoterol has more than 200-fold greater agonist activity at beta 2 -receptors than at beta 1 -receptors. Although beta 2 -receptors are the predominant adrenergic receptors in bronchial smooth muscle and beta 1 -receptors are the predominant receptors in the heart, there are also beta 2 -receptors in the human heart comprising 10% to 50% of the total beta-adrenergic receptors. The precise function of these receptors has not been established, but they raise the possibility that even highly selective beta 2 -agonists may have cardiac effects. The pharmacologic effects of beta 2 -adrenoceptor agonist drugs, including formoterol, are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3', 5'-adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. In vitro tests show that formoterol is an inhibitor of the release of mast cell mediators, such as histamine and leukotrienes, from the human lung. Formoterol also inhibits histamine-induced plasma albumin extravasation in anesthetized guinea pigs and inhibits allergen-induced eosinophil influx in dogs with airway hyper-responsiveness. The relevance of these in vitro and animal findings to humans with COPD is unknown.
acute deteriorations of chronic obstructive pulmonary diseaseasthmachronic obstructive pulmonary disease+1 more
2025
30
ISOPROTERENOL HYDROCHLORIDE
isoproterenol hydrochloride
Post-LOE
INJECTION · INJECTABLE
2025
30
LENALIDOMIDE
lenalidomide
Post-LOE
ORAL · CAPSULE
immunomodulatory, antiangiogenic, and antineoplastic properties. Cellular activities of lenalidomide are mediated through its target cereblon, a component of a cullin ring E3 ubiquitin ligase enzyme complex. In vitro, in the presence of drug, substrate proteins (including Aiolos, Ikaros, and CK1α) are targeted for ubiquitination and subsequent degradation leading to direct cytotoxic and immunomodulatory effects. Lenalidomide inhibits proliferation and induces apoptosis of certain hematopoietic tumor cells including MM and del (5q) myelodysplastic syndromes in vitro . Lenalidomide causes a delay in tumor growth in some in vivo nonclinical hematopoietic tumor models including MM. Immunomodulatory properties of lenalidomide include increased number and activation of T cells and natural killer (NK) cells leading to direct and enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) via increased secretion of interleukin-2 and interferon-gamma, increased numbers of NKT cells, and inhibition of pro-inflammatory cytokines (e.g., TNF-α and IL-6) by monocytes. In MM cells, the combination of lenalidomide and dexamethasone synergizes the inhibition of cell proliferation and the induction of apoptosis.
intermediate-1-risk myelodysplastic syndromes (MDS) associated with a deletion 5q cytogenetic abnormality withwithout additional cytogenetic abnormalitiesprogressed after two prior therapies+1 more
2025
30
LEVOCARNITINE
levocarnitine
Post-LOE
INJECTION · INJECTABLE
CLINICAL PHARMACOLOGY Levocarnitine is a naturally occurring substance required in mammalian energy metabolism. It has been shown to facilitate long-chain fatty acid entry into cellular mitochondria, thereby delivering substrate for oxidation and subsequent energy production. Fatty acids are utilized as an energy substrate in all tissues except the brain. In skeletal and cardiac muscle, fatty acids are the main substrate for energy production. Primary systemic carnitine deficiency is characterized by low concentrations of levocarnitine in plasma, RBC, and/or tissues. It has not been possible to determine which symptoms are due to carnitine deficiency and which are due to an underlying organic acidemia, as symptoms of both abnormalities may be expected to improve with Levocarnitine. The literature reports that carnitine can promote the excretion of excess organic or fatty acids in patients with defects in fatty acid metabolism and/or specific organic acidopathies that bioaccumulate acylCoA esters. Secondary carnitine deficiency can be a consequence of inborn errors of metabolism or iatrogenic factors such as hemodialysis. Levocarnitine may alleviate the metabolic abnormalities of patients with inborn errors that result in accumulation of toxic organic acids. Conditions for which this effect has been demonstrated are: glutaric aciduria II, methyl malonic aciduria, propionic acidemia, and medium chain fatty acylCoA dehydrogenase deficiency. Autointoxication occurs in these patients due to the accumulation of acylCoA compounds that disrupt intermediary metabolism. The subsequent hydrolysis of the acylCoA compound to its free acid results in acidosis which can be life-threatening. Levocarnitine clears the acylCoA compound by formation of acylcarnitine, which is quickly excreted. Carnitine deficiency is defined biochemically as abnormally low plasma concentrations of free carnitine, less than 20 µmol/L at one week post term and may be associated with low tissue and/or urine concentrations. Further, this condition may be associated with a plasma concentration ratio of acylcarnitine/levocarnitine greater than 0.4 or abnormally elevated concentrations of acylcarnitine in the urine. In premature infants and newborns, secondary deficiency is defined as plasma levocarnitine concentrations below age-related normal concentrations. End Stage Renal Disease (ESRD) patients on maintenance hemodialysis may have low plasma carnitine concentrations and an increased ratio of acylcarnitine/carnitine because of reduced intake of meat and dairy products, reduced renal synthesis and dialytic losses. Certain clinical conditions common in hemodialysis patients such as malaise, muscle weakness, cardiomyopathy and cardiac arrhythmias may be related to abnormal carnitine metabolism. Pharmacokinetic and clinical studies with Levocarnitine have shown that administration of levocarnitine to ESRD patients on hemodialysis results in increased plasma levocarnitine concentrations.
2025
30
PANTOPRAZOLE SODIUM
pantoprazole sodium
Post-LOE
INTRAVENOUS · INJECTABLE
(H, K)-ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus. The binding to the (H, K)-ATPase results in a duration of antisecretory effect that persists longer than 24 hours for all doses tested (20 mg to 120 mg).
2025
30
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Portfolio: 15 approved products
Top TAs: Oncology, Immunology, Infectious Diseases
Portfolio Health
Post-LOE15 (100%)
15 total products
Therapeutic Area Focus
Oncology
2 marketed
Immunology
1 marketed
Infectious Diseases
1 marketed
Rare Diseases
1 marketed
Respiratory
1 marketed
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