advanced glycation

ABR-238901 is an oral, active S100A8 A9 blocker that inhibits the interaction of S100A8 A9 with its receptors RAGE(receptor for advanced glycation end products) and TLR4 (toll-like receptor 4). ABR-238901 has potential as a compound for the treatment of myocardial infarction (MI).

Alagebrium chloride (ALT711) is an advanced glycation end product (AGE) inhibitor that has proven effective in reducing systolic blood pressure and providing therapeutic benefits for patients with diastolic.

Bromelain is an anti-inflammatory drug derived from pineapple stem. It acts through down-regulation of plasma kininogen, degradation of advanced glycation end-product receptors, inhibition of Prostaglandin E2 expression, and regulation of angiogenic bioma

Ipriflavone (Osteofix) (Osteofix) is a feed additive and a catabolic agent. It is used to inhibit bone resorption.

FPS-ZM1 is a high-affinity, RAGE-specific inhibitor that obstructs Aβ binding to the V domain of RAGE.

Tenilsetam (Piperazinone) is an endonuclease modulator; a nootropic agent and advanced glycation end product (AGE) inhibitor having potential for Alzheimer's disease (AD) treatment.

Homocarnosine acetate is a dipeptide unique to brain consisting of γ-aminobutyric acid (GABA) and histidine. Homocarnosine acetate has antioxidant and anti-inflammatory actions, prevention of DNA damage, and inhibition of advanced glycation end-product formation

Advanced glycation end products (AGEs) are compounds formed by non-enzymatic chemical reactions following the bonding of sugars to proteins or lipids during diabetes, uremia, aging, rheumatic arthritis, and other conditions. A receptor for the AGEs (RAGE) binds certain members of this class to initiate cell signaling.[1][2] Pentosidine is a well-characterized natural AGE that is often used as a biomarker for the production of all AGEs. While pentosidine can be measured in urine, the majority of this AGE is catabolized before excretion.[3] Reference:[1]. Neeper, M., Schmidt, A.M., Brett, J., et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. The Journal of Biological Chemisty 267(21), 14998-15004 (1992).[2]. Brett, J., Schmidt, A.M., Yan, S.D., et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. American Journal of Pathology 143(6), 1699-1712 (1993).[3]. Miyata, T., Ueda, Y., Horie, K., et al. Renal catabolism of advanced glycation end products: The fate of pentosidine. Kidney International 53, 416-422 (1998).

Advanced glycation end products (AGEs) are compounds that are produced through non-enzymatic chemical reactions when sugars bond with proteins or lipids, occurring in conditions such as diabetes, uremia, aging, and rheumatic arthritis. A specific receptor, known as RAGE, interacts with select AGEs to trigger cell signaling. Pentosidine, a prominently studied natural AGE, serves as a common biomarker for assessing AGE production. Although pentosidine levels can be determined through urine analysis, it is predominantly broken down prior to excretion.

Azeliragon (TTP488) is an antagonist at the Receptor for Advanced Glycation End products; is evaluated as a potential treatment for patients with mild-to-moderate Alzheimer_acute_s disease (AD).

Pyridoxylamine (pyridoxamine) is an inhibitor of advanced glycation end production (AGEs) and lipoxidation end products (ALEs).

LR-90, an advanced glycation end product (AGE) inhibitor, is utilized in diabetic animal model research. This compound effectively suppresses inflammatory responses in human monocytes.

Receptor for advanced glycation end products (RAGE) antagonist. Blocks S100P, S100A4 and HMGB-1 mediated RAGE activation in vitro and in vivo. Inhibits growth and metastasis of rat glioma tumors. Reduces cell growth and RAGE-mediated NF-κB activity in hum

Nε-(1-Carboxymethyl)-L-lysine (CML), an advanced glycation end product (AGE), is formed through the oxidative modification of glycated proteins under conditions of oxidative stress.1,2,3 Its levels escalate with age, diabetes, cancer, vascular diseases, and various pathologies associated with oxidative stress.1,4,5 CML interacts with the membrane-bound receptor for AGEs (RAGE), initiating signaling via MAPKs and NF-κB pathways. Conversely, a truncated version of RAGE generates a soluble protein that sequesters CML, thereby diminishing this signaling.6,7

NecroX-7 (LC-280126) is a potent free radical scavenger and HMGB1 (high-mobility group box 1) inhibitor. It serves as an antidote to acetaminophen toxicity and exerts a protective effect by preventing HMGB1 release in ischemia reperfusion injury. Additionally, NecroX-7 inhibits HMGB1-induced release of TNF and IL-6 and the expression of TLR-4 and receptor for advanced glycation end products. This compound may be used for graft-versus-host disease (GVHD) research [1].

Poliumoside is a natural compound which exhibits significant inhibition of advanced glycation end product formation with IC50 value of 4.6-25.7 μM, it also exhibits great inhibitory effects on rat lens aldose reductase with IC50 values of 0.85 μM.Poliumos

Rubrofusarin gentiobioside (Rubrofusarin-6-O-beta-D-gentiobioside) can significantly decrease the expression of TGF-beta1 and fibronectin and NF-kappaB DNA binding activity, suggests that it has potential as a preventive agent for advanced glycation end products-related diabetic complications.

Gemigliptin Tartrate (LC15-0444 tartrate) is a highly selective, reversible and competitive inhibitor of dipeptidyl peptidase-4 (DPP-4). It has an IC50 of 10.3 nM for human recombinant DPP-4. Gemigliptin tartrate exhibits potent anti-glycation properties.

Nε-(1-Carboxyethyl)-L-lysine (CEL), a known advanced glycation end product (AGE), forms through the interaction of methyl glyoxal and lysine residues within proteins. Unlike its free form, protein-bound CEL can attach to the receptor for AGEs (RAGE). Its concentrations are notably higher in the lenses of diabetic cataract patients and are reduced in rat heart mitochondria following sustained caloric restriction. Furthermore, at 1 mM, CEL impedes glutamate uptake and the release of S100B in rat hippocampal slices, an effect that occurs independently of RAGE.

3,5-Di-O-caffeoylquinic acid methyl ester exhibits potent inhibitory activities against the formation of advanced glycation end products (AGEs); it exhibits cytotoxicity actions against human cervix carcinoma HeLa cells. 3,5-Di-O-caffeoylquinic acid methyl ester shows high efficiency and low toxicity with antivirus activity against RSV.

Cassiaside C (Toralactone 9-O-β-D-gentiobioside), a naphthopyrone extracted from Cassia tora seeds, demonstrates in vitro inhibitory activity against the formation of advanced glycation end products (AGE).

Pimagedine is a prototype therapeutic agent for the prevention of formation of advanced glycation endproducts. Pimagedine reacts rapidly with α,β-dicarbonyl compounds such as methylglyoxal, glyoxal, and 3-deoxyglucosone to prevent the formation of advanced glycation endproducts (AGEs).

Alagebrium is a advanced glycation endproducts (AGE) cross-link breaker.

Homocarnosine TFA, a unique dipeptide of γ-aminobutyric acid (GABA) and histidine found in the brain, acts as an inhibitory neuromodulator synthesized from GABA within neurons. It exhibits anticonvulsant effects [1], and possesses antioxidant and anti-inflammatory properties, prevents DNA damage, and inhibits the formation of advanced glycation end-products [2].