Zilovertamab (UC-961) is a humanised monoclonal antibody against ROR1 that blocks Wnt5a-induced ROR1 signalling.

Roledumab (LFB-R593) is a human IgG1-κ antibody targeting RHD/CD240D. Roledumab is expressed by YB2/0 rat hybridoma cells.

Elezanumab (ABT-555; AE12-1Y-QL) is a human monoclonal antibody that selectively targets repulsive guidance molecule A (RGMa). Elezanumab potently inhibited RGMa mediated BMP signalling via the SMAD1/5/8 pathway, with an IC50 around 97 pM. Elezanumab promotes neuroregeneration and neuroprotection in neuronal injury and demyelination models binds N-terminal RGMa, blocks BMP signaling and lacks RGMc cross-reactivity. elezanumab has neuroregenerative and neuroprotective activities without impact on iron metabolism.

Rafivirumab (CR57) is an anti-rabies virus monoclonal antibody for the prophylaxis of rabies. Rafivirumab has neutralizing potency against a broad spectrum of RABV variants. Rafivirumab can be used for research of cocktails.

Foravirumab (CR4098) is a monoclonal antibody against rabies virus glycoprotein antigenic site III.

Cofetuzumab (PF-06523435) is a humanized IgG1-κ monoclonal antibody targeting PTK7. The expression system of Cofetuzumab is usually CHO (Chinese Hamster Ovary) cells.

Neihulizumab (ALTB-168) is an immune checkpoint agonistic antibody that binds to human CD162 (PSGL-1), leading to downregulation of activated T-cells. Neihulizumab can be uesd for steroid-refractory acute graft-versus-host-disease (SR-aGVHD), psoriasis, psoriatic arthritis and ulcerative colitis research.

Inclacumab (Anti-Human selectin P Recombinant Antibody) is a human monoclonal IgG4 antibody selectively targets P-selectin with a Kd value of 9.9 nM. Inclacumab inhibits P-selectin glycoprotein ligand 1 (PSGL-1) mimetic peptide bind with P-selectin with an IC50 value of 1.9 μg/mL and strongly inhibits cell adhesion.

Rolinsatamab is a IgG1κ type chimeric antibody targeting to PRLR (prolactin receptor). Rolinsatamab can be conjugated with pyrrolobenzodiazepine (PDB) dimer SGD-1882 (HY-101127) via a cleavable maleimidocaproyl type linker, to form an antibody-drug conjugate, Rolinsatamab talirine. One Rolinsatamab talirine has an average of 2 site-specific drug attachment engineered cysteines (C242, C242'). The linker equips the valine-alanine dipeptide, as cathepsine B cleavage site. on an average of 2 site-specific drug attachment engineered cysteines (C242, C242').

Sphingosine-1-phosphate (S1P) functions as a versatile signaling molecule, acting both intracellularly and extracellularly. Within cells, it serves as a secondary messenger, playing a key role in calcium ion (Ca²⁺) mobilization. Externally, S1P acts as a ligand, binding to and activating a range of G protein-coupled receptors, including S1P1-5 receptors as well as GPR3, GPR6, and GPR12. This bioactive lipid is synthesized from sphingomyelin and other membrane phospholipids, highlighting its importance as a critical mediator in various cellular processes.

GLS-15 is a novel GalNAc-derived small molecule structure designed for siRNA delivery.

THK-5475(THK5475) is a precursor of THK-5470, a monoamine oxidase-B(MAO-B) imaging probe, could be used for neurological diseases study (from patent EP2019-846498).

N-β-alanyldopamine hydrochloride, commonly referred to as NBAD hydrochloride, stands as the primary dopamine derivative found in haemolymph.

Alagebrium Chloride, identified as ALT711, emerged as a pioneering pharmaceutical candidate developed by Alteon, Inc. It marked the first clinical attempt to address the crosslinks formed by advanced glycation endproducts (AGEs), a key factor in the aging process. By targeting and disrupting these crosslinks, Alagebrium aims to counteract the stiffening of blood vessel walls, a condition linked to hypertension, cardiovascular disorders, and various age-related degenerative issues caused by protein crosslinking. Clinical studies have demonstrated its efficacy in lowering systolic blood pressure and offering therapeutic advantages for individuals with diastolic dysfunction.

Pemvidutide is a dual agonist targeting both GLP-1R and GCGR, demonstrating significant efficacy in reducing body weight, liver fat content, and serum lipid levels. Its unique mechanism of action makes it a promising candidate for research and therapeutic development in conditions such as non-alcoholic steatohepatitis (NASH) and obesity. This innovative compound offers potential for addressing complex metabolic disorders with a multifaceted approach.

HIFN​ (2-fluoro-N-(2-(5-hydroxy-1H-indol-3-yl)ethyl)nicotinamide) is a synthetic small-molecule agonist of the tropomyosin-related kinase B (TrkB) receptor, designed to mimic brain-derived neurotrophic factor (BDNF) signaling. Structurally, HIFN replaces the six-membered lactam ring of its parent compound HIOC with a fluoropyridine moiety, rendering it achiral and configurationally stable. This modification enhances binding affinity and pharmacokinetic properties. HIFN activates TrkB by inducing receptor dimerization and phosphorylation, triggering downstream survival pathways (PI3K/Akt, MAPK/Erk). In vitro, HIFN outperforms HIOC in TrkB activation (10 nM concentration) in primary neurons and NIH-3T3-TrkB cells. In vivo, systemic administration of HIFN (30–40 mg/kg) mitigates blast-induced retinal ganglion cell (RGC) degeneration and preserves visual function (contrast sensitivity, acuity) in mice for up to 8 weeks post-injury. Its effects are TrkB-dependent, as co-treatment with the TrkB antagonist ANA-12 abolishes neuroprotection. HIFN exhibits a critical therapeutic window of ≤3 hours post-injury and dose-dependent efficacy, with no toxicity observed at 600 mg/kg (acute) or 40 mg/kg/day (40-day chronic). Safety assessments reveal no histopathological or biochemical abnormalities in vital organs. By combining potent TrkB activation, blood-retina barrier penetration, and a robust safety profile, HIFN emerges as a promising therapeutic candidate for traumatic optic neuropathy and broader CNS disorders involving TrkB dysregulation.

JNJ-28583113 (JNJ28583113) a potent, selective, brain penetrant TRPM2 antagonist with IC50 of 126 nM (hTRPM2).JNJ-28583113 shows similar potency against species chimpanzee and rat TRPM2 with IC50 of 100 and 25 nM, respectively.JNJ-28583113 shows no significant (IC50>10 uM) reactivity towards PARP or PARG and a panel for multiple known kinases GPCRs and ion channels, nine other TRP channels with exception of TRPM5 (IC50<1 uM).Blocking TRPM2 via JNJ-28583113 caused phosphorylation of GSK3α and β subunits in cell assays.JNJ-28583113 also protected cells from oxidative stress induced cell death as well as morphological changes induced by non-cytotoxic concentrations of H2O2。JNJ-28583113 blunted cytokine release in response to pro-inflammatory stimuli in microglia.JNJ-28583113 was brain penetrant but not suitable for systemic dosing as it was rapidly metabolized in vivo, but the in-vitro pharmacology of JNJ-28583113 is the best in class.