Dr. Naikwadi College Of D. Pharmacy, Jamgaon, Sinnar- 422103.
SGLT2 inhibitors are a class of oral drugs that have had little efficacy in treating type 2 diabetes. Ertugliflozin and Dapagliflozin is a novel pharmaceutical treatment for type 2 diabetes patients and a fervent member of the sodium-glucose cotransporter-2 (SGLT2) family. Its primary objective is to reduce the risk of cardiovascular issues related to kidneys, the microvascular system, the macro vascular system, and diabetic mellitus (DM). It works by increasing the excretion of glucose in the urine rather than requiring insulin. These drugs’ direct effects on the kidneys represent a new paradigm in medical care. Scientific research has demonstrated that the usage of SGLT-2 inhibitors can lower the risk of cardiovascular disease (CVD) in India, but hypoglycemia is a minor problem. It’s important to understand how Ertugliflozin impacts the kidneys. In situations where stricter blood sugar control is required, the FDA advises raising the beginning dose from 5 mg once daily to 15 mg once daily, if the drug is well tolerated. Hypovolemia and urinary tract infections are two of ertugflozin’s most frequent side effects. Because of its synergistic action, Ertugliflozin can benefit individuals with type 2 diabetes when taken with other medications. The sodium glucose otransporte, which in found in the proximal nehron and is in charge of reintroducing filtered glucose into the bloodstream, is inhibited by it. By blocking this cotransporter, glucose recovery dereased, glucose excretion is increased, and hyperglycemia is decreased. The literature on Erugliflozin and Dapagliflozin’s action, effectiveness and clinical application is reviewed here.
Diabetes is the most serious health problem in the world. Chronically elevated blood glucose levels are the cause of this illness. Because they hinder the beta cells in the pancreas from either creating enough insulin or insulin that is either ineffective or malfunctions. Of the several types of diabetes, type 2 diabetes has been treated with limited effectiveness using a class of oral drugs called SGLT2 inhibitors. Ertugliflozin is a novel pharmaceutical treatment for type 2 diabetes patients and a fervent member of the sodiumglucose cotransporter-2 (SGLT2) family. Its main goal is to lessen the adverse effects of diabetes mellitus (DM).the heart system. It is a common consequence of uncontrolled diabetes and is characterized by an increase in blood glucose levels. Diabetes has been linked to an increased risk of lower respiratory tract infections, pneumonia, urinary tract infections, and soft skin infections, according to numerous research. Patients with diabetes who receive inadequate infection treatment are more likely to experience financial difficulties. Sodium-glucose cotransporter type-2 (SGLT2) inhibitors, as a novel class of hypoglycaemic drugs, are recommended for their favourable effects on patients with type 2 diabetes, especially for the established risk of cardiovascular or renal complications The first of this new family of treatments is dapagliflozin. The US Food and Drug Administration (FDA) granted it a license in January 2014. Ovid Medline (1946 to September 2014) search was Carried out using the terms “diabetes” and “dapagliflozin”. Papers and abstracts on animal studies and not in English Were excluded, including any duplicates (Figure 1). Any Useful references cited in these papers/abstracts were also Reviewed. A search on ClinicalTrials.gov using the search Term “dapagliflozin” was also made to find information on Past and ongoing studies. Other sources included the World Health Organization, the FDA, Centres for Disease Control And Prevention, clinical guidelines (including National Institute for Health and Care Excellence technology appraisal),FDA/EMA/UK labelling of summary of product characteristics, briefings, press releases, and Google search.
Ertugliflozin:
The novel medication Ertugliflozin, which is used to treat type 2 diabetes mellitus (T2DM), is a member of the sodium-glucose cotransporter-2 (SGLT2) family. The primary goal is to lessen diabetic complications that impact the cardiovascular, renal, microvascular, and macrovascular systems. The European Medicines Agency and the National Medical Product Administration were among the regulatory bodies in Europe and Asia that authorized or licensed Ertugliflozin, an oral medication used to help patients with type 2 diabetes mellitus (T2DM) control their blood glucose levels, on January 25, 2018.[1-2] Type 2 diabetes is becoming a major global health concern. Inhibiting SGLT2 can improve glucose excretion in the urine, and insulin alone lowers or blocks plasma glucose levels. Diabetic complications, such as coronary arteriosclerosis, diabetes acidosis, and hypoglycemia, pose serious health risks. The US Food and Drug Administration-approved drug Ertugliflozin, which is used to treat type 2 diabetes, is one highly specific inhibitor of class SGLT2.[3] SGLT2 inhibitors are a new class of oral medications that have been developed to treat type 2 diabetes. The drug classes that include canagliflozin, dapagliflozin, empagliflozin, and Ertugliflozin are as follows. Nowadays, Ertugliflozin is the most popular SGLT2 inhibitor.[4-5] Additionally, the organizations have approved the fixed dosage of the drug Ertugliflozin bioavailability of Ertugliflozin when taken orally is approximately 100%, and it reaches its peak concentration when the patient fasts for at least two hours after taking it. During treatment, the medication reaches a steady-state concentration in the body following an overdose. A half-life of 16.6 hours is also experienced by people with type 2 diabetes.[6] Since uridine diphosphate glutaronidasyltransferase (UGT)1A9 and UGT 2B7 catalyze Oglucuronidation, which transforms Ertugliflozin into two inert glucuronides, there is known to be minimal cytochrome P450-mediated metabolism of this drug.[7]
Ertugliflozin's Mechanism Of Action As A Sglt2 Inhibitor Drug:
SGLT2 inhibitors block SGLT2 in a selective manner.[8] The high capacity but low affinity SGLT2 transporters are found in the proximal convoluted renal tubule. They are in charge of 90% of the filtered plasma’s glucose being reabsorbed.Reducing hyperglycemia and encouraging the excretion of glucose in urine, blocking SGLT2 simply limits the kidneys’ capacity to reabsorb filtered glucose and salt.[9]
The IC50 values for the other medications were 684 nM for SGLT1 and 4.4 nM for SGLT2, while canagliflozin demonstrated significant cross-reactivity with SGLT1 in clinical trials. SGLT1 half-maximal inhibitory concentrations were lower for empagliflozin (1.6 mg), Ertugliflozin (1,960 mg), and dapagliflozin (803 mg) than for other SGLT2 inhibitors. Instead, sotagliflozin is a dual SGLT inhibitor, inhibiting both SGLT enzymes.[10] A new class of drugs called SGLT2 inhibitors directly targets the kidneys. And their activity is independent of insulin sensitivity. Hypoglycemia is a remote possibility, and pancreatic beta cell overstimulation is not a cause for alarm.[11] Additional effects of SGLT2 inhibition could include decreased weight, decreased albuminuria, changed lipid metabolism, increased haemoglobin levels, decreased oxygen consumption, and decreased cellular glucotoxicity. In addition to increasing mitochondrial activity. The levels of pro-inflammatory cytokines like IL-6, TNF, IFN, NF-, TLR-4, and TGF appear to be decreased by SGLT2 inhibitors.[12
Ertugliflozin’s Impact And Select Results On The Cardiovascular
One of the biggest challenges still facing diabetes is managing its effects, which include cardiovascular disease (CVD). Scientific research indicates that individuals with diabetes who are taking SGLT-2 inhibitors have a lower risk of cardiovascular disease (CVD). Therefore, medications that reduce blood sugar levels are obviously a significant improvement.[9] Insulin has little effect on the independent renal activity of SGLT-2 inhibitors that lower glucose levels, known as Glucosuria. As a result, they encourage weight loss instead of hypoglycemia. Reduced glucose toxicity enhances ß-cell function and insulin sensitivity.[10] Compared to the control group, patients using SGLT2 inhibitors had a significantly lower risk of atrial arrhythmias and end-cardiac events. Ventricular arrhythmias, commonly referred to as the “cardiac arrest” component of SCD, were significantly less common in both groups.[11]Patients with type 2 diabetes treated with SGLT2 inhibitors experienced fewer cardiac arrhythmias and failures.Further study is needed to determine whether the antiarrhythmic action of SGLT2 is medication- or class-specific.[12] In any case, type 2 diabetics were still far more likely than non-diabetics to die from cardiovascular (CV) events, although their rate was lower than that of controls.[12-13] It has been demonstrated in clinical studies that Ertugliflozin and empagliflozin, when compared to more recent types of SGLT-2 inhibitors, reduce the risk of cardiovascular problems in people with diabetes. In contrast with saxagliptin and linagliptin. Further investigation is necessary to determine the causes of heart failure and non-diabetic cardiac problems.[14] Ertugliflozin, dapagliflozin, empagliflozin, and canagliflozin’s cardiovascular effects were investigated in four extensive trials involving type 2 diabetes. The exams The effects of canagliflozin and empagliflozin on type 2 diabetes were examined in two studies: the CANVAS PROGRAMME (Canagliflozin Cardiovascular Assessment research) and the EMPAREG OUTCOME research.12-13-71 When Ertugliflozin was assessed statistically, it had no effect on the three major adverse cardiac events (MACEs) of nonfatal myocardial infarction, cardiovascular death, and nonfatal stroke. It was associated with a 30?crease in hospitalizations owing to heart failure.[7-14] By means of osmotic diuresis, Ertugliflozin protects the heart. Additionally, patients with heart failure may benefit from lower oxygen consumption as well as higher cardiac preload and afterload due to decreased plasma volume. As the haematocrit level increases, the heart muscle gets more oxygen. This rise may be caused by a decrease in plasma volume or an increase in erythropoietin synthesis. In addition to lowering weight and blood pressure, SGLT2 inhibitors have a number of beneficial benefits on the heart and metabolism.[5-16]
Renal
It's important to understand how Ertugliflozin impacts the kidneys. A series of metabolic alterations seem to have been triggered by the calorie deficit brought on by increased glucosuria and decreased glucotoxicity. If this is successful, it may protect the kidneys, arteries, retina, heart, and fat from oxidative stress, endothelial dysfunction, edema, and fibrosis. Ertugflozin’s capacity to restore glomerular feedback in tubules is what gives it its reno-protective properties. Consequently, there is a decrease in intra-glomerular pressure, shear force, albuminuria, hyperfiltration, and the proximal convoluted tubule’s reabsorption of glucose and salt.[17-18]
SGLT2 inhibitors have physiological effects beyond their impact on blood pressure and kidney function, such as natriuresis. Ertugliflozin reduces the albumin/creatinine ratio and lessens the risk of renal failure in individuals with type 2 diabetes who have developed diabetic nephropathy. The patient receives renal replacement therapy when their kidney fails, and their capacity to filter urine is greatly reduced (for example, their blood creatinine levels double or Their estimated glomerular filtration rate, or eGFR, falls by 40% over time.[19-20] With a mixed-status ertugliflozin population and a pre-planned exploratory composite renal endpoint analysis, David Z. I. Cherney et al. conducted a cohort trial using 5 mg and 15 mg of ertugliflozin. Additionally recorded are changes in albuminuria and albuminuria status over time, as well as changes in the therapy group’s eGFR. Every aspect of the population as a whole and subgroups based on baseline renal function were examined. Researchers looked at the frequency of adverse events linked to acute renal failure using two subgroups of baseline eGFR and the Acute Renal Failure Standard Medical Dictionary for Regulatory Activities Query (SMQ).It has also been found that ertugliflozin has renoprotective properties.[20] Type 2 diabetes mellitus can lead to a reduced glomerular filtration rate (GFR), chronic kidney disease (CKD), high blood pressure, heart disease, persistent albuminuria, and hypertension. SGLT2 inhibitors effectively reduce blood pressure when taken with antihypertensive medications. A growing body of literature indicates that multiple cardiovascular outcomes trials (CVOTs) have included renal endpoints. Suggesting that patients with type 2 diabetes may benefit from these medications’ reno-protective effects. Whether or not SGLT2 inhibitors have a therapeutic effect in reducing the evolution of kidney damage in people with type 2 diabetes will be clarified by numerous ongoing research looking at renal outcomes.[22-23]
Acceptances And Suggestions:
People whose blood sugar levels are controlled by type 2 diabetes may benefit from ertugliflozin when combined with other lifestyle modifications like regular exercise and a balanced diet. The medication was approved by the FDA in 2017 and the EMA in the first part of 2018. According to FDA guidelines, a dose greater than 5 mg once daily should be started. If greater glycemic control is needed, up to 15 mg once daily, as long as the drug is adequately tolerated. If your eGFR is less than 30 mL/min/1.73 m?2; or falls between 30 and 60 mL/min/1.73 m?2;, as stated in, don’t begin taking ertugliflozin.[24] The American Diabetes Association (ADA) recommends SGLT2 inhibitors for individuals with ASCVD, HF, and CKD concurrently. When A SCVD is prevalent, the AD A suggests a medication that blocks SGLT2, such as empagliflozin or canagliflozin, with good CV outcome evidence.[25]Three SGLT2 inhibitors with strong evidence of heart failure outcomes— canagliflozin, dapagliflozin, or empagliflozin—are recommended by the American Diabetes Association if heart failure is present.[25] Because of their beneficial effects on the kidneys, experts advise SGLT2 inhibitors like canagliflozin, dapagliflozin, or empagliflozin if chronic renal disease is a major concern. Since they all aid in delaying the progression of CKD.[25] The American Association of Clinical Endocrinologists and the American College of Endocrinology (AACE/ACE) released its most recent treatment guidelines for type 2 diabetes in 2020, and they highly recommend using medications that inhibit SGLT2. Heart failure (defined by a decreased ejection fraction) and cardiovascular disease (CVD) are more common in people with specific medical conditions: Since SGLT2 inhibitors have been shown to prevent CV events, they are used in stage 3 chronic kidney disease (CKD), also known as advanced ischemic heart disease (ASCVD).[26]. Because of their ability to lower the risk of cardiovascular and renal events, the SGLT2 inhibitors canagliflozin, dapagliflozin, and empagliflozin have been suggested here. It is their policy to refrain from recommending a specific SGLT2 inhibitor when there is no elevated risk due to cardiovascular disease or these known co-morbidities. It is advised to use SGLT2 medications with favourable cardiovascular and renal outcomes in place of alternativeSGLT2 inhibitors (such ertugliflozin) when their effects are neutral.
Adverse Effects
Ertugflozin’s safety as a monotherapy or combination treatment for type 2 diabetes has recently been evaluated in phase II trials. In a single ertugliflozin study, the highest number of cases of symptomatic hypoglycemia was 19.2% with glimepiride beginning dosage mg, 7– 10% with ertugliflozin mg, and 15 mg of 1 S ertugliflozin, respectively. Other adverse events included symptomatic hypoglycemia and GMIs in males (zero percent at 1 mg glimepiride, 2.1 percent at 5 mg ertugliflozin, and 4.4 percent at 15 mg ertugliflozin) and women (1.4 percent at 1 mg glimepiride, 7.7 percent at 5 mg ertugliflozin, and 10% at 15 mg ertugliflozin).[27]GMIs are the most common side effect in both sexes, according to clinical studies. Ertugliflozin users should be made aware of this side effect and closely monitored during their treatment. In the majority of clinical trials, the active treatment group saw a lower incidence of symptomatic hypoglycemia, UTIs, and hypovolemia compared to the placebo group. You can reduce your risk of symptomatic hypoglycemia by using insulin or sulfonylurea together with an SGLT2 inhibitor. SGLT2 inhibitors do not increase the risk of symptomatic hypoglycemia when taken with other blood sugar-lowering drugs. Based on the information at hand. Changing the dosage of diuretics and antihypertensive drugs in highrisk persons can treat rare episodes of hypovolemia. One canagliflozin trial reported amputation; however, no other SGLT2 inhibitor has shown this risk beyond observational evidence. Although a number of early observational studies reported acute renal injury, the most recent evidence supports the idea that SGLT2 inhibitors could protect the kidneys. Rarely, SGLT2 inhibitors can result in euglycemic diabetic ketoacidosis (DKA) in people with type 2 diabetes. According to one study, there are between 0.16 and 0.76 incidences of DKA for every 1000 patient years. “This contrasts with the findings of a canagliflozin experiment, which showed that 10% of those with type 1 diabetes who were subjected to SGLT2 inhibitors had DKA.[28] Clinical research has shown that ertugliflozin and other medications that lower blood pressure and help people lose weight are inhibitors of adverse effects.[29]
Conjunction Of Ertugliflozin With Other Medications:
Because of its synergistic action, ertugliflozin can benefit individuals with type 2 diabetes when taken with other medications. One such medication is sitagliptin, which is marketed alongside ertugliflozin under the brand name STEGLUJAN. The Biopharmaceutical Classification System classifies sitagliptin and ertugliflozin as class 1 drugs. When used together, these two antihyperglycemic medications lower blood sugar levels more efficiently than when taken separately because of their distinct but complementary mechanisms of action and outstanding safety profiles. For type 2 diabetics whose condition cannot be controlled with metformin alone, this strategy is expected to yield favourable clinical outcomes. Individuals with poorly managed type 2 diabetes who took ertugliflozin plus metformin experienced improvements in their weight reduction, hypertension, and glycemic control.[30]
Table 1: Merits and Demerits of Ertugliflozin
|
|
Merits of ertugliflozin |
Demerits of Ertugliflozin |
|
|
Heart and kidney protection |
Elevated levels of lowdensity lipoprotein |
|
|
lower blood pressure |
Blood sugar levels in the urine |
|
|
Lack of hypoglycemia risk |
Higher risk of ketoacidosis in diabetics |
Dapagliflozin:
Mechanism Of Action:
As early as 34 weeks of pregnancy, the human nephron may reabsorb nearly all of the glucose contained in the filtrate.[31,32] This amounts to 180 grams of glucose daily.[33,34] 90% of the filtered glucose is reabsorbed by SGLT2, which is expressed by the epithelial cells lining the first segment of the proximal convoluted tubule, while only 1% of the filtered glucose enters the urine. Lower in the nephron, SGLT1 reabsorbs the remaining 10%.SGLT2[35-36] actively transports glucose from the glomerular filtrate into the epithelial cells at the luminal surface of the proximal tubular epithelium, where the process of glucose reabsorption [37-40] begins. The active transport of sodium out of the basolateral cells by the Na+/K+-adenosine triphosphatase pump drives the cotransporters' movement of glucose and sodium. The passive transporters known as glucose transporters (GLUTs) transfer glucose over the basolateral membrane and out of the cell. Along the concentration gradient, this takes place. Glucose is returned to the circulation from the proximal tubule as a result of this entire process.
The functioning of the SGLT2/GLUT2 transporter molecules has been better understood thanks to two hereditary disorders[32]: Fanconi-Bickel syndrome and familial renal glycosuria.
Pharmacokinetic:
When dapagliflozin is taken orally, it is quickly and effectively absorbed.[41,42] Within two hours of dosing, dapagliflozin plasma concentrations reach their maximum (in the fasting state). The once-daily (OD) dosage of 10 mg has a 78% bioavailability. Taking it with or without food is possible.[43] 91% of it is protein-bound, and neither renal nor hepatic illness may alter this.
Uridine diphosphate-glucuronosyltransferase 1A9 is the enzyme that breaks down dapagliflozin in the liver and kidney to its inactive metabolite, dapagliflozin 3-O-glucuronide. Dapagliflozin has a mean plasma terminal half-life of 13 hours (10 mg dose). Renal impairment impairs the excretion of dapagliflozin and its metabolites, which are primarily eliminated through the urine.[44] 15% is eliminated unchanged by feces, and 2% is eliminated unchanged through pee.
Pharmacodynamic
Dapagliflozin is linked to increased diuresis of 375 mL/day on average [41,42,45,46]and dose-dependent glycosuria. Although there is a brief rise in sodium excretion in the urine, serum sodium levels do not seem to be impacted. The excretion of uric acid in the urine increases temporarily, whereas the levels of uric acid in the serum decrease with time. Glycosuriainduced uric acid release via GLUT9 isoform 2 in the proximal tubule or suppression of uric acid uptake at the collecting duct of the renal tubule [47] have been suggested as the causes of decreased serum uric acid levels, while the exact mechanism is unknown. Dapagliflozin’s ability to reduce weight may also be the cause of this.
Side Effects :
Urinary tract infections have also been reported [48]. For dapagliflozin 5mg, 10 mg, or placebo, urinary tract infections were reported in 5.7%, 4.3%, and 3.7% of patients, respectively. Again, these were mild or moderate infections that responded to standard oral antibiotic therapy. Therapy discontinuation for this reason was also rare (0.3% with dapagliflozin and 0.1% with placebo). There was no increase in serious infections, eg, pyelonephritis
Neither dapagliflozin monotherapy nor metformin dual treatment is linked to hypoglycemia. Compared to Sus, it is linked to lower hypoglycemia.[49] However, when dapagliflozin is used with other hypoglycemic medications, including insulin and Sus, there is a higher chance of hypoglycemia.[50] To lower the risk of hypoglycemia at the start of treatment, it is recommended that the dose of these medications be downtitrated when dapagliflozin is started.
With dapagliflozin therapy, volume depletion (dehydration, hypotension, or hypovolemia) seems to be rare. These were not statistically significant and were reported at 0.8% against 0.4% for dapagliflozin 10 mg OD versus placebo.
Dapagliflozin frequently causes back pain, disorientation, dyslipidemia, and a rise in hematocrit.[41]
Dapagliflozin Use In Patients With Liver, Kidney, And Heart Disease
Dapagliflozin’s glycemic improvement lasts in renal failure at least as far as stage 3 CKD (_>60 mL/min/1.73 m2).[51] Patients with more severe renal illness have not been screened for it. Additionally, therapy decreases blood pressure and causes weight reduction (-1.33 and -1.68 kg for 5 and 10 mg, respectively). Crucially, these patients’ renal function has not become any worse. As a result, patients with CKD stage 3A (45–59 mL/min/1.73 m2) may benefit somewhat, but only slightly. Longer-term research is necessary.
Liver illness is linked to T2D.[52,53] Ten milligrams of dapagliflozin have been tried in patients with various levels of liver damage. Liver-function testing showed no change, and it was well tolerated.[54] In clinical practice, mild to moderate hepatic impairment does not require a change in dosage. The manufacturers recommend a starting dose of 5 mg for patients with severe hepatic impairment. If the medicine is well tolerated, the dose may be increased to 10 mg.[41]
A comprehensive trial of older T2D patients with coexisting cardiovascular illness (964 individuals) demonstrated the safety and effectiveness of dapagliflozin.[55] Dapagliflozin helped the research participants lose weight, improved glycemic control without increasing hypoglycemia, and was well tolerated. These advantages lasted for 2 years.[56] This topic is being further examined by a research that is scheduled to conclude in April 2019 (Multicentre Trial to Evaluate the Effect of Dapagliflozin on the Incidence of Cardiovascular Events [DECLARE-TIMI58], ClinicalTrials.gov identifier: NCT01730534).The incidence of myocardial infarction, stroke, cardiovascular death, and all-cause death were reported to have decreased by 13.8%, 9.1%, 9.6%, and 5.0%, respectively, in a 20-year simulation study[57] that estimated the long-term cardiovascular and microvascular outcomes.
Dapagliflozin Use In Different Situations
There is currently one study that has examined dapagliflozin in type 1 diabetes (T1D). This was a randomized, double-blind, placebo-controlled, parallel-group, Phase II trial (ClinicalTrials.gov identifier: NCT01498185). It was designed to explore dapagliflozin (1, 2.5, 5, 10 mg OD) as an add-on to insulin therapy in subjects with T1D. A dose-dependent increase in urinary glucose and a reduction in glycemic levels/variability and total daily dose of insulin was noted with dapagliflozin. Hypoglycemia was noted to be common in all treatment groups, and led to discontinuation in one patient on dapagliflozin 10 mg OD due to a major hypoglycemic event.[58] Another gliflozin, empagliflozin, has been studied[59] in an open-label 8-week trial at a dose of 25 mg OD on renal hyperfiltration in T1D. Patients were divided into those with renal hyperfiltration (GFR_>135 mL/min/1.73m2, n=27) or normal GFR (GFR 90–134 mL/min/1.73m2, n=13). A statistically significant reduction in total daily dose of insulin and in HbA1c was observed in both study groups. There is therefore proof of concept for the use of SGLT2 inhibitors for the therapy of T1D.
Loop diuretics and dapagliflozin should not be taken simultaneously to prevent dehydration and hypotension. Simvastatin, valsartan, warfarin, digoxin, rifampin, and mefenamic acid have not been found to interact with dapagliflozin.[60,61]
CONCLUSION
Ertugliflozin, In December 2017, the FDA authorized ertugliflozin, a novel SGLT-2 inhibitor, for the treatment of adult type 2 diabetes mellitus. This insulin-dependent mechanism increases the excretion of glucose in the urine. Clinical studies have demonstrated that it is safe and enhances weight loss and A1C. Protecting the heart and kidneys is the main goal of lowering the risk of complications from diabetes mellitus. Ertugliflozin usage reduces the risk of adverse events in patients with cardiovascular disease and chronic renal sickness. Ertugliflozin can be used without aggravating pre-existing conditions such as heart disease or kidney disease if you have type 2 diabetes.
Dapaglifloin, The first class SGLT2 Inhibitor authorized for treatment in adult T2D patients is dapagliflozin. Numerous investigations have shown that this treatment has a glycemic advantage without causing appreciable hypoglycemia. Additionally, there are advantages with weight, cholesterol, and blood pressure that could have a positive impact on the heart. In any case, dapagliflozin significantly adds to the array of treatments we need for the best possible care of T2D patients. Regardless of remaining ?-cell function, its action is unaffected by a patient’s position in the natural history of diabetes. Additionally, it does not depend on the mechanisms of action of other oral hypoglycemia agents, such as lowering insulin resistance or gluconeogenesis, increasing glucose deposition into fat, muscle, or liver tissues, or slowing intestinal carbohydrate digestion and absorption
REFERENCES
Mansi Shelke*, Monali Khatake, Vishweshwari Bhagat, Nikita Pabale, Tanvi Kamble, An Overview of Ertugliflozin and Dapagliflozin in The Treatment of Diabetes Mellitus, Int. J. of Pharm. Sci., 2024, Vol 2, Issue 11, 1590-1602. https://doi.org/10.5281/zenodo.14242419
10.5281/zenodo.14242419
