Odronextamab is a hinge-stabilised, fully human IgG4-based CD20 × CD3 bispecific antibody that binds CD3 on T cells and CD20 on B cells[1].
Carotegrast is an orally available α4 integrin receptor inhibitor with anti-inflammatories activities.
S1PR-MO-1 is the modulator of sphingosine-1-phosphate receptor, used for research of hyperproliferative, inflammatory diseases.
Hyperforin is a transient receptor canonical 6 (TRPC6) channels activator. Hyperforin modulates Ca2+ levels by activating Ca2+-conducting non-selective canonical TRPC6 channels. Hyperforin also shows diverse pharmacological activities including anti-depression, anti-tumor, anti-dementia, anti-diabetes. Hyperforin modulates γδ T cells to secret IL-17α, improves Imiquimod (HY-B0180)-induced psoriasis-like mice model[1][2][3][4][5].
Resolvin E2 ((-)-Resolvin E2), a proresolving lipid mediator, is useful as a lead for anti-inflammatory agent[1].
Gnetumontanin B is a stilbenoid that can be found in Gnetum montanum f. megalocarpum. Gnetumontanin B inhibits TNF-α production with an IC50 value of 1.49 µM[1].
Galantide is a reversible and non-specific galanin receptor antagonist.
ADU-S100 ammonium salt is an activator of stimulator of interferon genes (STING).
Icariside F2 is a potent NF-κB inhibitor with an IC50 value of 16.25 μM. Icariside F2 is an aromatic glycoside isolated from the leaves of E. ulmoides Oliver. Icariside F2 has anti-inflammatory activity[1].
Cereblon modulator 1 (compound F) is a cereblon (CRBN) E3 ligase modulator. Cereblon modulator 1 specifically binds to CRBN, thereby affecting the activity of the ubiquitin E3 ligase complex. This leads to the ubiquitination of certain substrate proteins and induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3)[1][2].
α-Helical Corticotropin Releasing Factor (9-41) is a corticotropin releasing factor (CRF) antagonist. α-Helical Corticotropin Releasing Factor (9-41) decreases plasma growth hormone (GH) values in vivo[1][2].
BIBR 1087 SE is an intermediate metabolite of dabigatran etexilate.
Regaloside B is a phenylpropanoid isolated from Lilium longiflorum. Regaloside B can inhibit the expression of iNOS and COX-2, has anti-inflammatory activity[1][2].
GTS-21 dihydrochloride is a selective α7 nicotinic acetylcholine receptor agonist, has recently been established as a promising treatment for inflammation. Target: nAChRin vitro: GTS-21 is one of the most potent α7nAChR agonists, has been reported to attenuate pro-inflammatory cytokine production, improve outcomes in sepsis models, pancreatitis, and ischemia-reperfusion injury, and inhibit the production of endotoxin-induced TNF in lung tissue. In addition, recent studies have demonstrated that GTS-21 inhibits the activities of endothelial cells and monocyte macrophages, as well as the secretion of pro-inflammatory cytokines in peripheral blood samples, by regulating the JAK2-STAT3 pathway. [1] in vivo: In septic animals, GTS-21 significantly ameliorated GI motility, lowered systemic and colonic levels of IL-6, decreased colonic permeability, and decreased the number of positive cultures obtained from blood and mesenteric lymph nodes. Splenectomy prevented animals from developing sepsis-induced ileus. Chrna7 mice displayed a more severe septic phenotype, whereas GTS-21 remarkably was also beneficial in these animals. [2]
ACTH (1-13) is a 13-aa peptide, with cytoprotective effects in the model of ethanol induced gastric lesions in rats.
DHODH-IN-12 (Compound 12b) is a Leflunomide derivative and a weak dihydroorotate dehydrogenase (DHODH) inhibitor with a pKa of 5.07[1].
SB 239063 is a potent and selective p38 MAPK inhibitor (IC50 = 44 nM for p38α). SB 239063 displays > 220-fold selectivity over ERK, JNK1 and other kinases; ~ 3-fold more selective than SB 203580. IC50 value: 44 nM ( p38α)Target: p38 MAPKSB 239063 reduces inflammatory cytokine production and is neuroprotective following oral administration in vivo.
S 16474 is an antagonist of Neurokinin-1 Receptor.
Rabeprazole sodium(LY307640 sodium) is an antiulcer drug in the class of proton pump inhibitors.Target: Proton PumpRabeprazole belongs to a class of antisecretory compounds (substituted benzimidazole proton-pump inhibitors) that do not exhibit anticholinergic or histamine H2-receptor antagonist properties, but suppress gastric acid secretion by inhibiting the gastric H+/K+ATPase (hydrogen-potassium adenosine triphosphatase) at the secretory surface of the gastric parietal cell. Because this enzyme is regarded as the acid (proton) pump within the parietal cell, rabeprazole has been characterized as a gastric proton-pump inhibitor. Rabeprazole blocks the final step of gastric acid secretion. In gastric parietal cells, rabeprazole is protonated, accumulates, and is transformed to an active sulfenamide. When studied in vitro, rabeprazole is chemically activated at pH 1.2 with a half-life of 78 seconds.
Manfidokimab (AK120) is an anti-interleukin 4 receptor alpha (IL-4Rα) IgG4 monoclonal antibody[1].
UC-1V150 is a specific TLR7 (Toll-like receptor) agonist that stimulates cellular immune responses and has anti-tumor activity. UC-1V150 can be used to synthesize ISAC (Immune-Stimulating Antibody Conjugates) molecule[1][2].
p38 MAPK-IN-4 (compound 6) is a p38 MAPK inhibitor with an 50 of 35 nM[1].
(S)-Thalidomide ((S)-(-)-Thalidomide) is the S-enantiomer of Thalidomide. (S)-Thalidomide has immunomodulatory, anti-inflammatory, antiangiogenic and pro-apoptotic effects[1][2][3]. (S)-Thalidomide induces teratogenic effects by binding to cereblon (CRBN) [4].
2-[(4-Oxo-1,2,3-benzotriazin-3-yl)oxy]acetic acid (HBA) is a hapten with a carboxyl group at the end of its spacer arm, suitable for reacting with free amine groups of proteins. 2-[(4-Oxo-1,2,3-benzotriazin-3-yl)oxy]acetic acid can be combined with carrier proteins and used in antigen design[1].
K-7174 dihydrochloride is a novel cell adhesion inhibitor; inhibits the expression of vascular cell adhesion molecule-1 (VCAM-1) induced by either IL-1β or TNF-α.IC50 value:Target: GATA-specific inhibitorin vitro: K-7174 inhibited the expression of vascular cell adhesion molecule-1 (VCAM-1) induced by either tumor necrosis factor alpha or interleukin-1beta, without affecting the induction of intercellular adhesion molecule-1 or E-selectin. K-7174 had no effect on the stability of VCAM-1 mRNA.K-7174 did not influence the binding to any of the following binding motifs: octamer binding protein, AP-1, SP-1, ets, NFkappaB, or interferon regulatory factor [1]. Addition of 10 microM K-7174 rescued these inhibitions of Epo protein production and promoter activity induced by IL-1beta, TNF-alpha, or L-NMMA, respectively [2]. K-7174 had the potential to induce endoplasmic reticulum (ER) stress evidenced by induction of GRP78 and CHOP.Other inducers of ER stress completely reproduced the effects of K-7174 including suppression of lipid accumulation, blockade of induction of adiponection and PPARgamma and maintenance of MCP-1 expression [3].in vivo: K-7174, one of proteasome inhibitory homopiperazine derivatives, exhibits a therapeutic effect, which is stronger when administered orally than intravenously, without obvious side effects in a murine myeloma model. Moreover, K-7174 kills bortezomib-resistant myeloma cells carrying a β5-subunit mutation in vivo and primary cells from a patient resistant to bortezomib [4].
BMS-1166 hydrochloride is a potent PD-1/PD-L1 interaction inhibitor with an IC50 of 1.4 nM. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation.
Sodium lauroyl glutamate is an anionic amino acid surfactant. Sodium lauroyl glutamate has the irritant contact dermatitis potential, and possible anti-irritating potential in a surfactant mixture on human skin[1].
Ginkgetin is a natural biflavonoid isolated from leaves of Ginkgo biloba L; effects of anti-inflammation and anticancer have been reported.IC50 value:Target:in vitro: Ginkgetin inhibits COX-2 dependent phases of prostaglandin D(2) (PGD(2)) generation in bone marrow-derived mast cells (BMMC) in a concentration-dependent manner with IC(50) values of 0.75 microM. Ginkgetin consistently inhibited the production of leukotriene C(4) (LTC(4)) in a dose dependent manner, with an IC(50) value of 0.33 microM. Ginkgetin also inhibited degranulation reaction in a dose dependent manner, with an IC(50) value of 6.52 microM [1]. Ginkgetin inhibited both inducible and constitutively activated STAT3 and blocked the nuclear translocation of p-STAT3 in DU-145 prostate cancer cells. Furthermore, ginkgetin selectively inhibited the growth of prostate tumor cells stimulated with activated STAT3. Ginkgetin induced STAT3 dephosphorylation at Try705 and inhibited its localization to the nucleus, leading to the inhibition of expression of STAT3 target genes such as cell survival-related genes (cyclin D1 and survivin) and anti-apoptotic proteins (Bcl-2 and Bcl-xL) [2]. Ginkgetin suppressed the viability of PC-3 cells in a concentration-dependent manner and also significantly increased the sub-G1 DNA contents of cell cycle in PC-3 cells. Ginkgetin activated caspase-3 and attenuated the expression of survival genes such as Bcl-2, Bcl-xL, survivin and Cyclin D1 at protein and mRNA levels [3]. Ginkgetin (1 - 10 microM) and the biflavonoid mixture (10 - 50 microg/ml), mainly a 1 : 1 mixture of ginkgetin and isoginkgetin, from G. biloba leaves, inhibited production of prostaglandin E2 from lipopolysaccharide-induced RAW 264.7 cells [4].in vivo: Ginkgetin inhibited tumor growth in xenografted nude mice and down-regulated p-STAT3Tyr705 and survivin in tumor tissues [2]. At total doses of 1,000 microg/site on the dorsal skin (15 mm x 15 mm), ginkgetin inhibited prostaglandin E2 production by 65.6 % along with a marked suppression of COX-2 induction. In addition, ginkgetin and the biflavonoid mixture (100 - 1,000 microg/ear) dose-dependently inhibited skin inflammation of croton oil induced ear edema in mice by topical application [4].
8-CPT-Cyclic AMP (8-CPT-cAMP) sodium is a selective activator of cyclic AMP-dependent protein kinase (PKA). 8-CPT-Cyclic AMP sodium is also a potent inhibitor of the cyclic GMP-specific phosphodiesterase (PDE VA) with an IC50 of 0.9 μM. 8-CPT-Cyclic AMP sodium also inhibits PDE III and PDE IV with IC50Epac and is a potent Epac activator[1][2].
O-Acetylschisantherin L (Acetylschisantherin L) is a natural lignan, which exhibits inhibitory effects on LPS-induced NO production in BV-2 cells with an IC50 of 23.1 μM[1].