Visual System Disease

ML-7 hydrochloride is a selective and highly specific myosin light chain kinase (MLCK) inhibitor that acts as a trabecular meshwork (TM) relaxant. ML-7 hydrochloride enhances Quinocetone (HY-123581)-induced phosphorylation of ERK, p38 MAPK and JNK, attenuates Akt activation, and promotes apoptosis of hepatocellular carcinoma cells. ML-7 hydrochloride reduces Th2 cytokine secretion by inhibiting MLCK, while alleviating smooth muscle hyperplasia and collagen deposition. As a non-antibiotic adjuvant, ML-7 hydrochloride restores the sensitivity of drug-resistant bacteria to Tigecycline (HY-B0117). ML-7 hydrochloride can be used in research related to glaucoma, hepatocellular carcinoma, asthma, and Klebsiella pneumoniae infection.

Aminoguanidine (Pimagedine) hydrochloride is an inhibitor of diamine oxidase (DAO) and nitric oxide synthase (NOS). Aminoguanidine hydrochloride can reduce the formation of advanced glycation end products (AGEs). Aminoguanidine hydrochloride has a dose-dependent inhibitory effect on Doxorubicin (HY-15142)-induced cell apoptosis. Aminoguanidine hydrochloride has antioxidant properties. Aminoguanidine hydrochloride can be used in the research of diabetic nephropathy.

Eculizumab (Anti-Human C5, Humanized Antibody) is a long-acting humanized monoclonal antibody targeted against complement C5. Eculizumab inhibits the cleavage of C5 into C5a and C5b and inhibits deployment of the terminal complement system including the formation of membrane attack complex (MAC). Eculizumab prevents anti-ganglioside antibody-mediated neuropathy in mice. Eculizumab can be used in hemolysis studies.

Faricimab, an overall good safety and tolerability profile, is a bispecific antibody targeting Angiopoietin-2 (Ang-2) and vascular endothelial growth factor-A (VEGF-A). Faricimab prevents retinal vascular leakage, cell death and inflammation in retinal ischemia/reperfusion (I/R) injury and sCNV mouse models. Faricimab demonstrates statistically superior visual acuity gains versus Ranibizumab (HY-P9951). Faricimab can be used for retinal diseases, such as age-related macular degeneration (w-AMD), diabetic macular edema (DME) and macular edema following retinal vein occlusion (RVO).

Tetracaine (Amethocaine) is a sodium channel inhibitor and ryanodine receptor (RyR) inhibitor. Tetracaine blocks sodium conduction across nerve cell membranes, preventing rapid sodium ion influx and depolarization. Tetracaine exhibits biphasic effects on spontaneous sarcoplasmic reticulum Ca²⁺ release in Ca²⁺-overloaded ventricular myocytes, and increases sarcoplasmic reticulum Ca²⁺ load. Tetracaine can be used in research related to eye diseases.

Sphingomab (LT1002) is a mouse-derived IgG1 κ monoclonal antibody and also an inhibitor targeting S1P, with high affinity for S1P and a K_d value of 0.03 ± 0.002 nM. Sphingomab blocks S1P-mediated IL-8 release in ovarian cancer cells. Sphingomab exhibits anti-angiogenic activity in a mouse model of choroidal neovascularization. Sphingomab reduces peripheral blood lymphocyte counts. Sphingomab can be used in the research of ovarian cancer and age-related macular degeneration.

PCB-OAA is a biocompatible multivinyl polycarboxybetaine macromonomer and that exhibits anti-fouling activity. PCB-OAA can form a hydrogel in vitreous cavity and shows an appealing ability to prevent significantly inflammatory response, fibrosis and complications such as raised intraocular pressure, and cataract formation. PCB-OAA can be used for the research of vitreous substitution.

EYE1118 is an orally active, photoactivatable VEGFR2 inhibitor without acute hepatotoxicity. EYE1118 mediates light-enhanced inhibition via azide-functionalized receptor binding, and can utilize light-guided targeting to regulate its biodistribution in vivo. EYE1118 effectively inhibits angiogenesis, endothelial cell migration, VEGF-induced retinal leakage, and the size of choroidal neovascular lesions. EYE1118 has been applied in studies related to age-related macular degeneration, diabetic retinopathy, and choroidal neovascularization.

Xelafaslatide (ONL-1204) is a Fas receptor antagonist. Xelafaslatide blocks the Fas receptor signaling pathway and inhibits downstream apoptosis and inflammatory pathways. Xelafaslatide suppresses neuroinflammation and microglial activation in glaucoma models, protects retinal ganglion cells and prevents axonal degeneration. Xelafaslatide is applicable to relevant research on glaucoma.

Tivanisiran sodium (SYL1001 sodium) is a small interfering RNA (siRNA) targeting TRPV1 . Tivanisiran sodium induces the degradation of TRPV1 mRNA, thereby inhibiting protein synthesis. Tivanisiran sodium alleviates ocular discomfort and pain, and improves ocular hyperemia and tear quality. Tivanisiran sodium is applicable to research related to dry eye disease.

Tetrahydrocortisol is a metabolite of Hydrocortisone (HY-N0583) that fails to activate glucocorticoid receptor. Tetrahydrocortisol inhibits Dexamethasone (HY-14648)-induced formation of cross-linked actin networks. Tetrahydrocortisol acts as a synergist to enhance the activity of anticancer agents. Tetrahydrocortisol can be used in the research of primary open-angle glaucoma, ocular hypertension, lung cancer and breast cancer.

HTRA1-IN-1 is a potent and selective high temperature requirement A serine peptid 1 (HTRA1) inhibitor with an IC₅₀ of 13 nM. HTRA1-IN-1 can be used for the research of HTRA1-related diseases, such as age-related macular degeneration (AMD), osteoarthritis, and rheumatoid arthritis.

Cenupatide (UPARANT) is a uPAR and FPR antagonist with anti-angiogenic, anti-inflammatory, and vascular barrier regulatory activities, as well as high stability and resistance to enzymatic degradation in blood/plasma. Cenupatide blocks the uPAR-FPR interaction, reduces VEGF-induced phosphorylation levels of AKT, VEGFR-2, STAT3, JNK, p38 MAPK, ERK1/2, and NF-κB p65, and inhibits αvβ3 integrin activation. Cenupatide suppresses endothelial cell migration, invasion, tube formation, and angiogenic signaling pathways, restores tight junctions and blood-retinal barrier integrity, reduces pro-inflammatory marker levels, and inhibits apoptosis. Cenupatide reduces retinal neovascularization, renal fibrosis, and vascular leakage, and restores visual function in preclinical models. Cenupatide is applicable to research related to retinopathy, diabetic complications, ocular diseases, cancer, and inflammatory diseases.

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.

Wheat Germ Agglutinin (WGA) Fluorescein is a classic fluorescent label that specifically binds to sugar residues such as N-acetylglucosamine, N-acetylneuraminic acid and sialic acid. Wheat Germ Agglutinin Fluorescein performs regionally differential fluorescent staining of the ocular surface epithelial glycocalyx to assess its integrity, and causes no damage to the eye at safe concentrations. Wheat Germ Agglutinin Fluorescein is also used for staining structures including red blood cells, cultured cells, bacteria and pine wood nematodes, and facilitates the isolation of wheat-associated plant-growth-promoting rhizobacterial strains. Wheat Germ Agglutinin Fluorescein can be applied to the detection of ocular glycocalyx integrity and the research of related diseases such as pine wilt disease.

Clemastine (HS-592; Meclastine) is an orally active, blood-brain barrier-permeable H1 histamine receptor (H1 histamine receptor) antagonist with potent antiallergic effects. Clemastine also antagonizes muscarinic acetylcholine receptors (mAChR), particularly the M1 and M4 subtypes. In addition to antihistamine effects, Clemastine exhibits multiple pharmacological activities, especially in promoting central nervous system remyelination, activating autophagy and pyroptosis, exerting anti-apoptotic and neuroprotective effects, and suppressing inflammation.

JB-1, an IGF-I analog, is a selective IGF-I receptor inhibitor that does not interact with IGF-II. JB-1 competes with IGF-I for binding to IGF-1R and blocks receptor autophosphorylation. JB-1 increases the level of sVEGFR-1. JB-1 normalizes retinal abnormalities, including reducing retinal neovascularization. JB-1 is applicable to studies related to oxygen-induced retinopathy.

Latanoprostene bunod (NCX116; LBN) is a nitric oxide-releasing prostaglandin F₂α analog. Latanoprostene bunod is a prodrug that, upon instillation into the eye, is hydrolyzed by corneal esterases into two active metabolites: Latanoprost (HY-B0577) and NO. Latanoprost activates the prostaglandin FP receptor to increase the outflow of aqueous humor through the uveoscleral pathway. NO increases aqueous humor drainage through the trabecular meshwork pathway, achieving synergistic enhancement targeting the dual pathways of aqueous humor outflow. Latanoprostene bunod can be used in research related to open-angle glaucoma and ocular hypertension.

Medrysone (HMS; 6α-Methyl-11β-hydroxyprogesterone) is a STAT6 modulator and M2 macrophage polarization inducer. Medrysone enhances IL-4-triggered STAT6 activation, upregulates the expression of M2 markers, and promotes the secretion of VEGF and CCL2. Medrysone also enhances the pro-migratory activity of M2-like macrophages toward endothelial cells. By regulating macrophage polarization and related repair pathways, Medrysone significantly promotes corneal wound repair in a rat mechanical injury model. Medrysone can be used for research related to corneal injury.

TREM-1 inhibitory peptide GF9 (Human TREM-1 (213-221)) is a TREM-1 inhibitor. TREM-1 inhibitory peptide GF9 blocks the TREM-1 signaling pathway via a ligand-independent mechanism, spontaneously inserts into the cell membrane to dissociate TREM-1 from DAP-12, and functions through the Signaling Chain Homooligomerization (SCHOOL) model. TREM-1 inhibitory peptide GF9 reduces the levels of TNFα, IL-1β, IL-6, and M-CSF. TREM-1 inhibitory peptide GF9 inhibits tumor growth, prolongs the survival of mice with pancreatic cancer models, ameliorates collagen-induced arthritis, and exerts protective effects on bone and cartilage simultaneously. TREM-1 inhibitory peptide GF9 can be used in research related to arthritis, pancreatic cancer, retinopathy, alcoholic liver disease, and liver cancer.