FAROGLIP S 50

Indications

• Major depressive disorder
• Generalized anxiety disorder
• Panic disorder
• Obsessive-compulsive disorder
• Post-traumatic stress disorder
• Menopausal symptoms (off-label)

Dosage

Adults: Initially 20 mg daily, increased in steps of 10 mg as necessary, maximum 40 mg per day for depressive illness. For panic disorder, initially 50–100 mg daily, increased gradually, maximum 300 mg per day.

Mechanism of action

Paroxetine enhances serotonergic activity by inhibiting the presynaptic reuptake of serotonin via the serotonin transporter (SERT). This inhibition increases serotonin levels in the synaptic cleft, alleviating symptoms associated with mood and anxiety disorders. It has a higher selectivity for serotonin reuptake inhibition compared to other SSRIs like citalopram and fluoxetine. While the mechanism for its effects on menopausal symptoms is not fully understood, it may relate to its influence on thermoregulation.

Pharmacodynamics

Paroxetine effectively treats symptoms of depression, anxiety disorders, obsessive-compulsive disorder, and post-traumatic stress disorder through serotonin reuptake inhibition. Its therapeutic effects typically begin to manifest around 6 weeks after initiation of treatment. Due to its serotonergic properties, there is a risk of serotonin syndrome, particularly when combined with monoamine oxidase inhibitors (MAOIs). A two-week interval is recommended before initiating paroxetine following MAOI treatment.

Pharmacokinetics

Paroxetine is well-absorbed after oral administration, with a peak plasma concentration occurring in approximately 4 to 8 hours. It is extensively metabolized in the liver via the cytochrome P450 2D6 pathway to various metabolites. The elimination half-life is approximately 21 hours, and it is excreted primarily in urine. Dose adjustments may be required in patients with hepatic or renal impairment.

Contra-indications

• Hypersensitivity to paroxetine or any of its ingredients
• Use with monoamine oxidase inhibitors (MAOIs) within 2 weeks
• Pregnancy, especially in the first trimester due to increased risk of congenital malformations

Adverse effects

• Common: Nausea, dry mouth, dizziness, insomnia, somnolence, sweating, sexual dysfunction
• Uncommon: Diabetic control impaired, blurred vision
• Rare: Acute glaucoma, hepatic disorders, peripheral edema
• Very rare: Neuroleptic malignant-like syndrome, bone fracture

Interactions

• Moderate: Increased exposure when used with procyclidine
• Increased exposure when used with second-generation antipsychotics, asenapine, and terbinafine
• Risk of serotonin syndrome when co-administered with other serotonergic agents, particularly MAOIs

Precautions

• Use with caution in patients with hepatic or renal impairment
• Monitor for serotonin syndrome, especially when used with other serotonergic drugs
• Gradual reduction of dose is recommended upon cessation to avoid withdrawal symptoms

Pregnancy

Increased risk of congenital malformations, especially if used in the first trimester. Caution is advised.

Breast-feeding

Present in breast milk but the amount is too small to be harmful. Nevertheless, caution is advised.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets: 10 mg, 20 mg, 30 mg, 40 mg
• Oral suspension: dosage forms available from special-order manufacturers

Indications

• Dehydration
• Fluid replacement
• Support for metabolic reactions
• Regulation of body temperature

Dosage

Children: Fluid requirements for children depend on age, weight, and activity level. It is crucial to monitor hydration status and adjust intake accordingly, referring to specific guidelines in the BNF for Children.

Adults: Dosage varies based on individual needs, activity level, and environmental conditions. General guidelines suggest approximately 2 to 3 liters per day for adults, considering factors like exercise and climate.

Mechanism of action

Water acts as a solvent in biological systems, enabling the dissolution and transport of nutrients and waste products. It also plays a vital role in metabolic reactions, including hydrolysis and dehydration synthesis, which are essential for cellular function.

Pharmacodynamics

Water maintains cellular integrity and supports physiological functions, including osmotic balance, acid-base equilibrium, and thermoregulation. Its role in enzymatic reactions and as a medium for biochemical processes is crucial for organismal health.

Pharmacokinetics

Water is absorbed efficiently in the gastrointestinal tract and distributed throughout the body via the bloodstream. It is excreted primarily through urine, sweat, and respiration. The body regulates water balance through mechanisms involving the kidneys, hormones, and thirst responses.

Pregnancy

Considered safe for use.

Breast-feeding

Considered safe for use.

Storage

Store in a cool, dry place away from sunlight.

Formulations

• Liquid
• Pure Water

Indications

• Used as a disintegrant in tablet formulations
• Enhances the bioavailability of active pharmaceutical ingredients

Dosage

Children: Refer to the specific formulation guidelines, as dosage will vary based on the active ingredient and formulation type.

Adults: Refer to the specific formulation guidelines, as dosage will vary based on the active ingredient and formulation type.

Mechanism of action

Croscarmellose sodium works by swelling and absorbing water when it comes into contact with gastrointestinal fluids. This swelling leads to the rapid disintegration of the tablet or capsule matrix, facilitating the release and absorption of the active pharmaceutical ingredients.

Pharmacodynamics

Croscarmellose sodium is classified as a superdisintegrant. Its ability to rapidly disintegrate solid dosage forms can significantly enhance the dissolution rate of the active ingredient, which is crucial for achieving therapeutic effects in a timely manner.

Pharmacokinetics

Croscarmellose sodium is not absorbed in the gastrointestinal tract and does not exert pharmacological effects in the body. It is considered non-toxic and is excreted unchanged. Its main role is as an excipient, influencing the formulation's characteristics rather than the pharmacokinetics of the active ingredients.

Precautions

• Use with caution in patients with known hypersensitivity to croscarmellose or its components.

Pregnancy

Safety in pregnancy has not been established. Use only if clearly needed.

Breast-feeding

Caution is advised when using during breastfeeding, as safety has not been established.

Storage

Store in a cool, dry place, away from moisture and heat.

Formulations

• Powder
• Granules

Dosage

Children: Refer to specific formulations and clinical guidelines for dosing information as this can vary widely based on the context of use.

Adults: Refer to specific formulations and clinical guidelines for dosing information as this can vary widely based on the context of use.

Mechanism of action

Dibasic compounds often act by providing a buffering effect in biological systems, which helps to maintain physiological pH levels. They may also interact with various biological targets depending on their specific structure, influencing metabolic pathways and cellular functions.

Pharmacodynamics

The pharmacodynamics of dibasic compounds is highly variable and depends on their specific chemical structure and the context of their use. Generally, these compounds may alter the absorption and distribution of other drugs, modulate enzyme activity, or affect cellular signaling pathways through their interactions with biological molecules.

Pharmacokinetics

The pharmacokinetics of dibasic compounds can vary widely. Factors such as solubility, stability, and route of administration influence their absorption, distribution, metabolism, and excretion. Typically, dibasic compounds may be absorbed in the gastrointestinal tract and may undergo various metabolic processes depending on their specific nature.

Pregnancy

Dibasic compounds should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult with a healthcare provider.

Breast-feeding

Caution is advised when administering dibasic compounds to breastfeeding mothers. Consult with a healthcare provider.

Storage

Store in a cool, dry place away from light. Keep out of reach of children.

Indications

• Dry eye syndrome
• Ocular surface disorders
• Eye irritation
• Contact lens discomfort

Dosage

Children: Refer to specific product instructions for paediatric dosage, as recommendations can vary widely based on age and clinical condition.

Adults: Refer to specific product instructions for adult dosage, which may vary based on formulation and severity of symptoms.

Mechanism of action

Insta works primarily by lubricating the ocular surface, which helps to alleviate dryness and discomfort. The active ingredients often mimic natural tears, providing moisture and aiding in the maintenance of the tear film, thereby improving eye comfort and visual clarity.

Pharmacodynamics

The pharmacodynamics of Insta involve the interaction of its components with the ocular surface, enhancing tear film stability and reducing the symptoms of dryness. The formulation may also reduce inflammation and irritation by providing a protective barrier over the eye.

Pharmacokinetics

The pharmacokinetics of Insta can vary depending on its specific formulation. Generally, the components are designed for local action, with minimal systemic absorption. The onset of action is typically rapid, with effects lasting for a variable duration depending on the specific formulation and the severity of symptoms.

Pregnancy

Consult a healthcare provider before use, as safety in pregnancy has not been established.

Breast-feeding

Consult a healthcare provider before use, as it is unknown if it is excreted in human milk.

Storage

Store in a cool, dry place away from direct sunlight.

Indications

• Eczema
• Atopic dermatitis
• Contact dermatitis
• Psoriasis
• Dry skin
• Skin irritation

Dosage

Children: For children, apply as directed by a healthcare provider, typically 1-3 times daily, depending on the severity of the condition and age of the child.

Adults: Apply generously to the affected area as needed, usually 1-3 times daily or as directed by a healthcare provider.

Mechanism of action

Moistshield works by forming a protective layer over the skin, preventing transepidermal water loss and maintaining hydration. It may also contain emollients that soften the skin and occlusive agents that trap moisture, thereby aiding in the restoration of the skin barrier. The specific ingredients can enhance skin repair and reduce inflammation.

Pharmacodynamics

The pharmacodynamic properties of Moistshield are primarily related to its ability to hydrate the skin and restore the skin barrier function. Emollients and occlusive agents in the formulation help to alleviate dryness and irritation, promoting overall skin health. The effectiveness can vary depending on the specific formulation and concentration of active ingredients.

Pharmacokinetics

Moistshield is applied topically, and its pharmacokinetics involve minimal systemic absorption. The active ingredients primarily act locally at the site of application. The onset of action is typically rapid, providing immediate relief from dryness and irritation. The duration of effect can depend on the formulation and frequency of application.

Pregnancy

Consult a healthcare provider before use during pregnancy.

Breast-feeding

Consult a healthcare provider before use while breastfeeding.

Storage

Store in a cool, dry place away from direct sunlight.

Dosage

Children: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Adults: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Mechanism of action

The mechanism of action for purified compounds varies widely depending on the specific substance. Generally, purified drugs exert their effects by interacting with specific biological targets, such as receptors, enzymes, or ion channels, leading to a desired therapeutic effect. This interaction can involve binding to receptors to activate or inhibit signaling pathways, modulating enzymatic activity, or altering physiological processes.

Pharmacodynamics

Pharmacodynamics describes the effects of a drug on the body and the relationship between drug concentration and effect. For purified drugs, this can involve dose-response relationships and the time course of their action. The purified form often enhances potency and reduces variability in response among patients, which can lead to more predictable therapeutic outcomes. The overall effect is determined by the drug's affinity for its target, the efficacy of the drug-receptor interaction, and the downstream signaling pathways activated as a result of this interaction.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of a drug. For purified substances, absorption can be more efficient due to the absence of impurities that may affect solubility or stability. Distribution may also be enhanced, leading to higher bioavailability. Metabolism can be influenced by the structure of the purified compound, as it may be metabolized more readily by liver enzymes. Excretion typically occurs through the kidneys or liver, depending on the molecular characteristics of the purified drug.

Pregnancy

Consult with a healthcare professional, as the safety of purified forms of medications during pregnancy may vary depending on the specific substance.

Breast-feeding

Consult with a healthcare professional, as the safety of purified forms of medications during breastfeeding may vary depending on the specific substance.

Storage

Store in a cool, dry place, away from light and moisture, and keep out of reach of children.

Indications

• Type 2 diabetes mellitus as monotherapy (if metformin is inappropriate)
• Type 2 diabetes mellitus in combination with other antidiabetic drugs (including insulin) when metformin alone or in combination fails to achieve adequate glycemic control

Dosage

Adults: 100 mg once daily, or 50 mg twice daily when used in combination with a sulfonylurea or insulin. Dose adjustments may be required based on renal function.

Mechanism of action

Sitagliptin inhibits the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for the degradation of incretin hormones. This inhibition results in prolonged active incretin levels, which enhances insulin secretion from pancreatic beta cells and decreases glucagon secretion from alpha cells in the pancreas, leading to lowered blood glucose levels.

Pharmacodynamics

Sitagliptin's pharmacodynamic effects include improved glycemic control, characterized by reduced fasting and postprandial blood glucose levels. The drug is effective in lowering HbA1c levels and is associated with a low risk of hypoglycemia. It has a beneficial effect on weight management, as it typically does not promote weight gain.

Pharmacokinetics

Sitagliptin is absorbed rapidly after oral administration, with peak plasma concentrations occurring within 1-4 hours. Its bioavailability is approximately 87%. The drug is predominantly eliminated via renal excretion, with about 80% of the dose excreted unchanged in the urine. The elimination half-life is approximately 12.4 hours. Renal impairment may necessitate dose adjustments, as clearance is significantly reduced in patients with decreased renal function.

Contra-indications

• History of pancreatitis
• Severe heart failure

Adverse effects

• Headache
• Constipation
• Dizziness
• Skin reactions
• Angioedema
• Back pain
• Cutaneous vasculitis
• Joint disorders
• Myalgia
• Acute pancreatitis
• Acute renal impairment
• Stevens-Johnson syndrome
• Vomiting

Interactions

• Concomitant use with sulfonylureas or insulin may require dose adjustments
• Moderate interaction with vemurafenib (increases exposure)

Precautions

• Monitor renal function before treatment and periodically thereafter
• Discontinue if symptoms of acute pancreatitis occur, such as persistent severe abdominal pain

Pregnancy

Avoid-toxicity observed in animal studies.

Breast-feeding

Avoid-present in milk in animal studies.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Tablets: 50 mg, 100 mg

Indications

• Dietary supplement
• Energy source
• Cosmetic ingredient
• Food additive

Dosage

Children: Refer to established dietary guidelines and consult nutritional resources for specific doses.

Adults: Refer to established dietary guidelines and consult nutritional resources for specific doses.

Mechanism of action

Stearic acid primarily acts as a source of energy. Once ingested, it undergoes beta-oxidation in the mitochondria, resulting in the production of acetyl-CoA, which enters the citric acid cycle to generate ATP. Stearic acid can also influence lipid metabolism and may impact cell membrane fluidity due to its role in phospholipid composition.

Pharmacodynamics

Stearic acid has a neutral effect on serum cholesterol levels compared to other saturated fatty acids. It does not raise low-density lipoprotein (LDL) cholesterol and may even have a beneficial effect on high-density lipoprotein (HDL) cholesterol levels. Its impact on metabolism includes promotion of lipogenesis and inhibition of lipolysis, contributing to energy homeostasis.

Pharmacokinetics

Stearic acid is absorbed in the gastrointestinal tract and transported via chylomicrons in the lymphatic system. It is metabolized primarily in the liver and muscle tissues. The half-life of stearic acid in the body varies depending on dietary intake and metabolic demands, and it is excreted as carbon dioxide and water through various metabolic pathways.

Pregnancy

Consult a healthcare professional before use, as safety during pregnancy is not established.

Breast-feeding

Consult a healthcare professional before use, as safety during breastfeeding is not established.

Storage

Store at room temperature, away from light and moisture.

Indications

• Nutritional supplement
• Support for cardiovascular health
• Source of essential fatty acids
• Antioxidant support

Dosage

Children: Refer to dietary guidelines for appropriate intake amounts based on age and dietary needs.

Adults: Refer to dietary guidelines for appropriate intake amounts, generally 1-2 tablespoons of sunflower oil as part of a balanced diet.

Mechanism of action

The primary constituents of sunflower seeds include polyunsaturated fatty acids, especially linoleic acid, vitamin E, and phytosterols. These compounds may exert beneficial effects on cardiovascular health by lowering LDL cholesterol levels and improving overall lipid profiles. The antioxidant properties of vitamin E help to reduce oxidative stress and inflammation.

Pharmacodynamics

Sunflower oil is known for its anti-inflammatory and antioxidant properties. The fatty acids in sunflower oil can modulate inflammatory pathways and may contribute to improved heart health by promoting endothelial function and reducing lipid peroxidation. The presence of vitamin E plays a crucial role in protecting cell membranes from oxidative damage.

Pharmacokinetics

Sunflower oil is primarily absorbed in the gastrointestinal tract. After ingestion, fatty acids are transported via chylomicrons to the lymphatic system and into the bloodstream. The metabolism of sunflower oil involves beta-oxidation in the liver, where fatty acids are converted into energy. The elimination half-life of sunflower oil components varies depending on the specific fatty acid, but generally, they are incorporated into various biological membranes and tissues.

Adverse effects

• Allergic reactions
• Gastrointestinal upset
• Skin rashes

Precautions

• Use with caution in individuals with allergy to ragweed or related plants
• May affect blood sugar levels in diabetic patients

Pregnancy

Sunflower seeds and oil are generally considered safe during pregnancy when used in food amounts. However, high doses should be avoided.

Breast-feeding

Sunflower oil is considered safe during breastfeeding, but it is advised to consume in moderation.

Storage

Store in a cool, dry place away from direct sunlight. Keep the container tightly closed.

Formulations

• Sunflower oil
• Sunflower seed

Mechanism of action

Paroxetine enhances serotonergic activity via the inhibition presynaptic reuptake of serotonin by the serotonin (SERT) receptor. This inhibition raises the level of serotonin in the synaptic cleft, relieving various symptoms. This drug has been demonstrated to be a stronger inhibitor of serotonin reuptake than other members of the same drug class, including [Citalopram], [Fluoxetine], and [Fluvoxamine]. The mechanism of action of paroxetine in relieving the vasomotor symptoms of menopause is unknown, according to the Brisdelle prescribing information, but may occur due to its effects on thermoregulation. Paroxetine shows a clinically insignificant affinity for adrenergic alpha-1 and alpha-2 receptors and β-adrenergic receptors, dopamine D1 and D2 receptors, histamine H1 receptors and serotonin 5-HT1A, 5-HT2A and 5-HT2C receptors. This drug shows some affinity for muscarinic cholinergic receptors and 5-H2B receptors. The delayed onset of paroxetine therapeutic effects may be explained by the initial paroxetine actions on the 5-HT neurons. In rats, paroxetine activates 5-HT1A receptors when it is first administered, inhibiting the stimulation of the 5-HT neurons and subsequent release of serotonin at the synaptic cleft. Functional and structural approaches were used to examine the inhibitory mechanisms and binding site location for fluoxetine and paroxetine, two serotonin selective reuptake inhibitors, on nicotinic acetylcholine receptors (AChRs) in different conformational states. The results establish that: (a) fluoxetine and paroxetine inhibit h alpha1beta1 gammadelta AChR-induced Ca(2+) influx with higher potencies than dizocilpine. The potency of fluoxetine is increased approximately 10-fold after longer pre-incubation periods, which is in agreement with the enhancement of (3)H-cytisine binding to resting but activatable Torpedo AChRs elicited by these antidepressants, (b) fluoxetine and paroxetine inhibit the binding of the phencyclidine analog piperidyl-3,4-(3)H(N)]-(N-(1-(2 thienyl)cyclohexyl)-3,4-piperidine to the desensitized Torpedo AChR with higher affinities compared to the resting AChR, and (c) fluoxetine inhibits (3)H-dizocilpine binding to the desensitized AChR, suggesting a mutually exclusive interaction. This is supported by our molecular docking results where neutral dizocilpine and fluoxetine and the conformer of protonated fluoxetine with the highest LUDI score interact with the domain between the valine (position 13') and leucine (position 9') rings. Molecular mechanics calculations also evidence electrostatic interactions of protonated fluoxetine at positions 20', 21', and 24'. Protonated dizocilpine bridges these two binding domains by interacting with the valine and outer (position 20') rings. The high proportion of protonated fluoxetine and dizocilpine calculated at physiological pH suggests that the protonated drugs can be attracted to the channel mouth before binding deeper within the AChR ion channel between the leucine and valine rings, a domain shared with phencyclidine, finally blocking ion flux and inducing AChR desensitization. Paroxetine was shown to be a potent (Ki = 1.1 nM) and specific inhibitor of [3H]-5-hydroxytryptamine (5-HT) uptake into rat cortical and hypothalamic synaptosomes in vitro. Lineweaver-Burk kinetic analysis determined that this inhibition was competitive in nature, implying a direct interaction with the 5-HT uptake transporter complex. Oral administration of paroxetine produced a dose-related inhibition of [3H]-5-HT uptake (ED50 = 1.9 mg/kg) into rat hypothalamic synaptosomes ex vivo with little effect on [3H]-l-noradrenaline (NA) uptake (ED50 greater than 30 mg/kg). This selectivity for 5-HT uptake was maintained after oral dosing for 14 days. Paroxetine (ED50 1-3 mg/kg PO) prevented the 5-HT depleting effect of p-chloroamphetamine (PCA) in rat brain, demonstrating 5-HT uptake blockade in vivo. Radioligand binding techniques in rat brain in vitro showed that paroxetine

Pharmacodynamics

Paroxetine treats the symptoms of depression, various anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, and the vasomotor symptoms of menopause via the inhibition of serotonin reuptake. The onset of action of paroxetine is reported to be approximately 6 weeks. Due its serotonergic activity, paroxetine, like other SSRI drugs, may potentiate serotonin syndrome. This risk is especially high when monoamine oxidase (MAO) inhibitors are given within 2 weeks of paroxetine administration. Upon cessation of MAO inhibitors, a 2-week interval before paroxetine administration is recommended. Do not coadminister these agents.

Mechanism of action

Inhibition of DPP-4 by sitagliptin slows DPP-4 mediated inactivation of incretins like GLP-1 and GIP. Incretins are released throughout the day and upregulated in response to meals as part of glucose homeostasis. Reduced inhibition of incretins increase insulin synthesis and decrease glucagon release in a manner dependant on glucose concentrations. These effects lead to an overall increase in blood glucose control which is demonstrated by reduced glycosylated hemoglobin (HbA1c). Januvia is a member of a class of oral anti-hyperglycemic agents called dipeptidyl peptidase 4 (DPP-4) inhibitors. The improvement in glycemic control observed with this medicinal product may be mediated by enhancing the levels of active incretin hormones. Incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are released by the intestine throughout the day, and levels are increased in response to a meal. The incretins are part of an endogenous system involved in the physiologic regulation of glucose homeostasis. When blood glucose concentrations are normal or elevated, GLP-1 and GIP increase insulin synthesis and release from pancreatic beta cells by intracellular signaling pathways involving cyclic AMP. Treatment with GLP-1 or with DPP-4 inhibitors in animal models of type 2 diabetes has been demonstrated to improve beta cell responsiveness to glucose and stimulate insulin biosynthesis and release. With higher insulin levels, tissue glucose uptake is enhanced. In addition, GLP-1 lowers glucagon secretion from pancreatic alpha cells. Decreased glucagon concentrations, along with higher insulin levels, lead to reduced hepatic glucose production, resulting in a decrease in blood glucose levels. The effects of GLP-1 and GIP are glucose-dependent such that when blood glucose concentrations are low, stimulation of insulin release and suppression of glucagon secretion by GLP-1 are not observed. For both GLP-1 and GIP, stimulation of insulin release is enhanced as glucose rises above normal concentrations. Further, GLP-1 does not impair the normal glucagon response to hypoglycemia. The activity of GLP-1 and GIP is limited by the DPP-4 enzyme, which rapidly hydrolyzes the incretin hormones to produce inactive products. Sitagliptin prevents the hydrolysis of incretin hormones by DPP-4, thereby increasing plasma concentrations of the active forms of GLP-1 and GIP. By enhancing active incretin levels, sitagliptin increases insulin release and decreases glucagon levels in a glucose-dependent manner. In patients with type 2 diabetes with hyperglycemia, these changes in insulin and glucagon levels lead to lower hemoglobin A1c (HbA1c) and lower fasting and postprandial glucose concentrations. The glucose-dependent mechanism of sitagliptin is distinct from the mechanism of sulfonylureas, which increase insulin secretion even when glucose levels are low and can lead to hypoglycemia in patients with type 2 diabetes and in normal subjects. Sitagliptin is a potent and highly selective inhibitor of the enzyme DPP-4 and does not inhibit the closely-related enzymes DPP-8 or DPP-9 at therapeutic concentrations. Sitagliptin is a DPP-4 inhibitor, which is believed to exert its actions in patients with type 2 diabetes by slowing the inactivation of incretin hormones. Concentrations of the active intact hormones are increased by Januvia, thereby increasing and prolonging the action of these hormones. Incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are released by the intestine throughout the day, and levels are increased in response to a meal. These hormones are rapidly inactivated by the enzyme, DPP-4. The incretins are part of an endogenous system involved in the physiologic regulation of glucose homeostasis. When blood glucose concentrations are normal or elevated, GLP-1 and GIP increase insulin synthesis and release from pancreatic beta cells by

Pharmacodynamics

Sitagliptin inhibits DPP-4 which leads to increased levels of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide(GIP), decreased levels of glucagon, and a stronger insulin response to glucose.