Diabetes|Inhibitors Agonists Modulators Antagonists|HmoBio.com

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Diabetes mellitus is a metabolic condition characterized by an inability to regulate blood glucose levels. It is caused by either defects in insulin production and secretion (Type I) or defects in insulin signaling (Type II). As of 2000 at least 2.8% of the worlds population suffer from diabetes.

Type I Diabetes

Type I diabetes, previously known as insulin-dependent or juvenile diabetes, is usually due to autoimmune attack of β-islet cells in the pancreas. It can also be idiopathic and there is increasing evidence of a viral etiology. The normal function of β-islet cells is to produce insulin in response to elevated blood glucose, which in turn promotes the conversion of glucose into glycogen polymers for storage. Destruction of β-islet cells prevents insulin production and subsequently manifests as hyperglycemia.

Genetic susceptibility genes for type I diabetes have been identified and include IDDM1, which codes for a MCH II complex that is displayed on the surface of β-islet cells. Certain polymorphisms of this gene result in the display of improper antigens on the surface of β-cells, leading to their targeting for destruction by T-cells.

Type II Diabetes

Type II diabetes, previously known as non-insulin-dependent or obesity-related diabetes, is characterized by insulin resistance and a loss of insulin sensitivity. Insulin levels may be increased (hyperinsulinemia) or decreased (hypoinsulinemia). Other factors that contribute include decreased activity of glucose transporters, increased hepatic glucose production and delayed β-cell sensitivity to hyperglycemia. The etiology of type II diabetes is unknown, but it is associated with obesity (particularly central obesity), sedentary lifestyle, high sugar diet, total body irradiation (a cancer treatment), hypertension and increasing age.

Pharmacological Interventions

First line treatment for type I diabetes is insulin replacement therapy. Type II diabetes is initially treated by attempts to maintain glycemic control with diet modifications. Pharmacological interventions, such as metformin, are used later. Diabetic complications are prevalent and uncontrolled so there is intense interest in developing pharmacological agents that allow better management of this condition. Novel antidiabetic treatments include fibroblast growth factor-21 analogs, renal sodium-glucose transporter inhibitors, free fatty acid receptor ligands, dipeptidyl peptidase IV (DPP-IV) inhibitors and more.

Cat. No.	Product Name	CAS No.	Information
H9508	Omzotirome	1092551-88-6	Omzotirome is a novel functional analog of iodothyronines, reduces adiposity by increasing energy expenditure and fatty acid oxidation in rats receiving a high-fat diet.
H9496	LY3502970	2212020-52-3	LY3502970 is an orally active nonpeptide GLP-1R agonist.
H9306	Retagliptin phosphate	1256756-88-3	Retagliptin phosphate (SP2086 phosphate) is a selective, competitive and orally active dipeptidyl peptidase-4 (DPP-4) inhibitor. Retagliptin phosphate can be used for type 2 diabetes mellitus (T2DM) research.
H9305	Retagliptin	1174122-54-3	Retagliptin (SP2086) is a selective, competitive and orally active dipeptidyl peptidase-4 (DPP-4) inhibitor. Retagliptin can be used for type 2 diabetes mellitus (T2DM) research.
H8985	Avexitide acetate	2051593-46-3	Avexitide acetate is a first in class glucagon like peptide-1 (GLP-1) receptor antagonist
H8984	Avexitide	133514-43-9	Avexitide is a first in class glucagon like peptide-1 (GLP-1) receptor antagonist
H8929	Azemiglitazone	1133819-87-0	MSDC-0602 is a PPARγ-sparing thiazolidinedione (TZD), interacts with the mitochondrial pyruvate carrier (MPC) and inhibits its activity and has the potential for type 2 diabetes study with reducing risk of PPARγ-mediated side effects.
H8738	Enavogliflozin	1415472-28-4	Enavogliflozin (DWP 16001) is an orally available, small molecule, sodium glucose transporter 2 inhibitor
H6944	ZLN-024 hydrochloride	1883548-91-1	A novel AMPK allosteric activator that has no effect on mitochondrial function or the ADP/ATP ratio; directly activate recombinant AMPK α1β1γ1 and its homologue α2β1γ1 with EC50 of 0.42 uM and 0.95 uM, respectively; also directly activate recombinant AMPK α1β2γ1 (EC50=1.1 µuM) and AMPK α2β2γ1 (EC50=0.13 uM); activates AMPK in L6 myotubes and stimulates glucose uptake and fatty acid oxidation; improves glucose tolerance, liver tissue weight, triacylglycerol and decreases the total cholesterol content in db/db mice (15 mg/kg/day).
H6943	ZLN-024	723249-01-2	A novel AMPK allosteric activator that has no effect on mitochondrial function or the ADP/ATP ratio; directly activate recombinant AMPK α1β1γ1 and its homologue α2β1γ1 with EC50 of 0.42 uM and 0.95 uM, respectively; also directly activate recombinant AMPK α1β2γ1 (EC50=1.1 µuM) and AMPK α2β2γ1 (EC50=0.13 uM); activates AMPK in L6 myotubes and stimulates glucose uptake and fatty acid oxidation; improves glucose tolerance, liver tissue weight, triacylglycerol and decreases the total cholesterol content in db/db mice (15 mg/kg/day).

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