Brazikumab (AMG 139) is a human IgG2 monoclonal antibody, selectively binds the p19 subunit of IL-23, with a KD of 0.138 nM for human IL-23. Brazikumab can be used for the research of Crohn's disease[1].
Semapimod tetrahydrochloride (CNI-1493), an inhibitor of proinflammatory cytokine production, can inhibit TNF-α, IL-1β, and IL-6. Semapimod tetrahydrochloride inhibits TLR4 signaling (IC50≈0.3 μM). Semapimod tetrahydrochloride inhibits p38 MAPK and nitric oxide production in macrophages. Semapimod tetrahydrochloride has potential in a variety of inflammatory and autoimmune disorders[1][2][3].
[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P, a Substance P derivative, is a biased agonist toward neuropeptide and chemokine receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P activates G12. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P binds to IL-8 and GRP receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P inhibits ERK-2 activation, activates JNK activity. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P stimulates an increase in neutrophil migration and Ca2+ mobilization. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P is also a bombesin antagonist, and inhibits the growth of small cell lung cancer[1][2][3]
Tebentafusp (IMCgp100) is a bispecific fusion protein to target gp100 peptide-HLA-A*02:01 (a melanoma-associated antigen). Tebentafusp guides T cells to kill gp100-expressing tumor cells via a high affinity T-cell receptor (TCR) binding domain and an anti-CD3 T-cell engaging domain. Tebentafusp leads to inflammatory cytokines and cytolytic proteins production, resulting in the direct lysis of tumour cells[1][2].
Muscone is the main active monomer of traditional Chinese medicine musk. Muscone inhibits NF-κB and NLRP3 inflammasome activation. Muscone remarkably decreases the levels of inflammatory cytokines (IL-1β, TNF-α and IL-6), and ultimately improves cardiac function and survival rate[1].
CC-90002 is a humanized anti-CD47 monoclonal antibody (mAb). CC-90002 has a high affinity for binding to CD47 with a subnanomolar Kd value. CC-90002 can be used for the research of hematologic malignancies and solid tumors[1][2].
Anti-inflammatory agent 35 (compound 5a27) is an orally active curcumin analogue with anti-inflammatory activity. Anti-inflammatory agent 35 blocks mitogen-activated protein kinase (MAPK) signaling and p65 nuclear translocation of NF-kB. Anti-inflammatory agent 35 also inhibits yellow neutrophil infiltration and pro-inflammatory cytokine production. Anti-inflammatory agent 35 significantly attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI) in vivo[1].
Gamma-glutamylcysteine (TFA) ((γ-glutamylcysteine (TFA)), an intermediate in glutathione (GSH) synthesis, is a dipeptide served as an essential cofactor for the antioxidant enzyme glutathione peroxidase (GPx). Gamma-glutamylcysteine (TFA) also upregulates the level of the anti-inflammatory cytokine IL-10 and reduces the levels of the pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and attenuates the changes in metalloproteinase activity in oligomeric Aβ40-treated astrocytes[1].
Balsalazide could suppress colitis-associated carcinogenesis through modulation of IL-6/STAT3 pathway.
Tyrphostin A1(AG9) inhibits CD40L-stimulated IL-12 production in macrophage cultures and antigen-induced generation of Th1 cells.IC50 value: Target: IL-12 production inhibitorAddition of increasing concentration of A1 resulted in a dose dependent decrease of IL-12 p40, with maximal inhibition (62.5%) occurring at a dose of 10 μM. tyrphostin A1 blocks CD40L-induced translocation of NF-κB to the nucleus, and reduces the activation of IL-12 p40 gene. In vivo therapy with A1 leads to decrease in generation of myelin basic protein (MBP) specific encephalitogenic T cells. In addition, treatment of SJL/J mice with A1 results in attenuation of experimental allergic encephalomyelitis (EAE) [1]. Tyrphostin A1 is a much weaker inhibitor of TK than other tyrphostins (IC50>1250 μM for epidermal growth factor receptor (EGFR) kinase), and therefore often used to differentiate TK-mediated effects of tyrphostins from other non-specific effects [2].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
Interleukin II (60-70) is a 60-70 fragment of the cytokine Interleukin II polypeptide[1].
Xeligekimab (GR 1501) is an anti-human interleukin 17A (IL-17A) humanized monoclonal antibody. Xeligekimab inhibits the pro-inflammatory cascade[1].
Veledimex S enantiomer is the S enantiomer of veledimex. Veledimex is an oral activator ligand for a proprietary gene therapy promoter system, and a moderate inhibitor of and substrate for CYP3A4/5.
Manfidokimab (AK120) is an anti-interleukin 4 receptor alpha (IL-4Rα) IgG4 monoclonal antibody[1].
Camoteskimab (AVTX-007) is a fully human, high-affinity anti-IL-18 monoclonal antibody. Camoteskimab has the potential for the autoinflammatory diseases research, including adult-onset Still’s disease (AOSD)[1].
IL-17 modulator 8 (compound 286) is an orally active modulator of IL-17. IL-17 modulator 8 significantly reduces IL-6, IFN-γ, and edema. IL-17 modulator 8 can used in study arthritis[1].
Ligufalimab (AK 117) is a humanized IgG4 anti-CD47 monoclonal antibody. Ligufalimab does not induce RBC hemagglutination, and induces phagocytosis. Ligufalimab shows anti-tumor activity[1].
VGX-1027(GIT27) is an isoxazole compound that exhibits various immunomodulatory properties; reduce the secretion of IL-1beta, TNF-alpha and IL-10 from purified murine macrophages.IC50 value: Target: immunomodulatorAdministration of VGX-1027 to NOD mice with spontaneous or accelerated forms of diabetes induced either by injection of cyclophosphamide or by transfer of spleen cells from acutely diabetic syngeneic donors markedly reduced the cumulative incidence of diabetes and insulitis. In addition, VGX-1027 given either i.p. or p.o. to CBA/H mice made diabetic with multiple low doses of streptozotocin successfully counteracted the development of destructive insulitis and hyperglycemia [1]. VGX-1027 appeared to spare T cell function as it was unable to modify the proliferation and/or secretion of IL-2, IFN-gamma and IL-4 induced in purified murine CD4+ T cells from stimulation with either CD3+CD28 or ConA [2]. VGX-1027 inhibited both proliferation of enterobacterial antigen-reactive CD4+CD25- T cells in vitro and the development of clinical and histological signs of colitis in vivo [3].
Lipoxin A4 (LXA4), an endogenous lipoxygenase-derived eicosanoid mediator, has potent dual pro-resolving and anti-inflammatory properties[1]. Lipoxin A4 inhibits proliferation and inflammatory cytokine/chemokine production of human epidermal keratinocytes (NHEKs) associated with the ERK1/2 and NF-kB pathways[2]. Lipoxin A4 inhibits serum amyloid A (SAA)-mediated IL-8 release with an IC50 value of 25.74 nM[3].
Naphazoline (Naphthazoline) is a potent α-adrenergic receptor agonist. Naphazoline reduces vascular hyperpermeability and promotes vasoconstriction. Naphazoline reduces the levels of inflammatory factors (TNF-α, IL-1β and IL-6), cytokines (IFN-γ and IL-4), IgE, GMCSF, and NGF。Naphazoline can be used for non-bacterial conjunctivitis research[1][2].
LMT-28 (LMT28) is a specific blocker of IL-6 signaling via inhibits IL-6Rβ (gp130) with IC50 of 5.9 uM (IL-6–induced luciferase activity), selectively inhibits IL-6–induced phosphorylation of STAT3, JAK2, and gp130; does not affect LIF-induced STAT3 activation and not inhibit IL-11 stimulation on HepG2 cells; binds directly and specifically to gp130, and thereby inhibits the interaction of gp130 with the IL-6/IL-6Rα complex; inhibits IL-6–induced proliferation of the human erythroleukemic cell line TF-1 with IC50 of 7.5 uM; inhibits IL-6–induced TNF-α production, ameliorates the progression of pancreatitis in mice.
Denileukin diftitox (DAB 389IL-2) is a diphtheria toxin (DT)-related interleukin 2 (IL-2) fusion protein toxin that depletes cells expressing the high-affinity form of the IL-2 receptor (IL-2R), CD25. Denileukin diftitox binds to cells expressing IL-2R and inhibits protein synthesis through internalization of the diphtheria toxin fragment[1][2][3].
Lib2-1, a macrocyclic peptide, is an IL-17C/IL-17RE interaction inhibitor. Lib2-1 can be used for autoimmune and inflammatory diseases research[1].
Gumokimab (AK 111) is a monoclonal antibody targeting IL-17A, which can be used in the study of psoriasis, ankylosing spondylitis. Gumokimab competitively blocks the binding of human IL-17A to IL-17R.
(R)-TCB2 is the R-enantiomer of TCB2. TCB2 is a potent anti-human interleukin-2 antibody, facilitates heterodimeric IL-2 receptor signaling and improves anti-tumor immunity[1].
IL-17 modulator 4 is a prodrug of IL-17 modulator 1 (HY-141535). IL-17 modulator 1 is an orally active, highly efficacious IL-17 modulator[1].
Tucotuzumab (Anti-EPCAM Recombinant Antibody) is a protein composed of an IgG1 monoclonal antibody specific for the human Epithelial Cell Adhesion Molecule (EpCAM) antigen, linked to two molecules of IL-2. Tucotuzumab is an immunosuppressant and antineoplastic agent[1].
Lebrikizumab is an IgG4 humanized monoclonal antibody that specifically binds to interleukin-13 (IL-13) and inhibits its function. Lebrikizumab can be used for the research of asthma[1].