JWG-045 is a selective ERK5 inhibitor. JWG-045 exhibits unique ferroptosis-resistant activity independent of ERK5 inhibition. JWG-045 can be used in breast cancer research.

JRN73958 is a PI3K/Akt, MAPK, and NF-κB inhibitor. JRN73958 decreases LPS/IFNγ-induced PI3K/Akt, MAPK, and NF-κB activity. JRN73958 can be used for the research of leukemia.

JRC-I-191 is an anti-HIV-1 agent. JRC-I-191 inhibits HIV-1 YU-2 entry into cells. JRC-I-191 does not inhibit infection of cells by amphotropic murine leukemia virus. JRC-I-191 can be used for the research of HIV-1 infection.

JNUTS013 is a NLRP3 inflammasome inhibitor. JNUTS013 promotes proteasome-dependent degradation of NLRP3 and inhibits the release of downstream cytokines. JNUTS013 downregulates the expression of inflammation-related proteins including iNOS and COX-2. JNUTS013 exhibits anti-inflammatory activity and can be used in the research of inflammatory diseases.

JNK-IN-17 (Compound 9J) is a selective and potent JNK inhibitor with IC50 values of 0.039, 0.079 μM for JNK1 and JNK3. JNK-IN-17 can inhibit c-Jun phosphorylation with an IC50 of 0.082 μM in Streptozotocin-infuced INS-1 pancreatic islet β cells. JNK-IN-17 shows inhibition rate ≤ 33% on the four main P450 subtypes (2C9, 2D6, 3A4, 1A2) in human liver microsomes, indicating a relatively low risk of drug interactions. JNK-IN-17 can be used for researches of neurological and metabolic disease, such as Parkinson's disease.

JNK3-IN-10 is a blood-brain barrier-impermeable JNK3 inhibitor (IC50=0.257 nM) with over 400-fold selectivity over JNK1. JNK3-IN-10 blocks the JNK3-mediated signaling pathway downstream of TGF-β1, inhibits TGF-β1-induced phosphorylation of c-Jun, reduces the expression of pro-fibrotic markers, and restores the expression of the epithelial protein E-cadherin. JNK3-IN-10 exhibits low cytotoxicity, anti-fibrotic, cytoprotective and renoprotective effects, and alleviates albuminuria, glomerulosclerosis and podocyte foot process fusion. JNK3-IN-10 can be used for the research of chronic kidney disease, glomerulosclerosis and adriamycin-induced nephropathy.

JNK2/MKK7 PPI-IN-1 is an orally active JNK2 inhibitor with an IC50 of 0.99 μM and a Kd of 81.6 μM. JNK2/MKK7 PPI-IN-1 inhibits JNK2 kinase activity, disrupts JNK2-MKK7 protein-protein interaction, and reduces c-Jun phosphorylation. JNK2/MKK7 PPI-IN-1 inhibits LPS-induced overexpression of inflammatory cytokines IL-6 and TNF-α. JNK2/MKK7 PPI-IN-1 can be used for the research of acute lung injury.

JNK1 ligand-1 (Compound P1) is a selective JNK1 inhibitor. JNK1 ligand-1 can be used as a JNK1 ligand to synthesize a series of PROTAC molecules, such as PROTAC JNK1-targeted-1. PROTAC JNK1-targeted-1 can be used for the research of pulmonary fibrosis.

NTM-006 is a selective and brain-penetrant adenosine A3 receptor (A3AR) agonist. NTM-006 selectively interacts with adenosine A3AR via π-π stacking with Phe168 and π-alkyl interactions receptor residues. NTM-006 inhibits Acetic acid-induced writhing responses in mice. NTM-006 can be used for the research of chronic neuropathic pain, cancer-related pain, osteoarthritis-associated pain.

JI-101 hydrochloride is an orally active angiogenesis inhibitor and anticancer agent with 55% oral bioavailability in Sprague Dawley rats, high permeability, and no P-gp substrate activity.JI-101 hydrochloride modulates angiogenesis signaling pathways in tumor vessel beds, downregulates EphB4, targets EphB4, VEGFR-2, and PDGFR-β, and inhibits multiple stages of tumor angiogenesis.JI-101 hydrochloride exerts activity against cancer cells and xenografts, exhibits mild to moderate inhibition of CYP3A4, and shows stability in pre-clinical and human liver microsomes.JI-101 hydrochloride undergoes rapid oral absorption in Sprague Dawley rats, has extensive tissue distribution with preferred lung uptake, and is excreted via bile with mono- and di-hydroxy metabolites, with feces as the primary elimination route.JI-101 hydrochloride can be used for the research of ovarian cancer and solid tumors.

JHU-58 is a peptidomimetic agonist targeting mouse MRGPRC11 and rat MRGPRC receptors. JHU-58 demonstrates analgesic effects in mouse models of neuropathic pain. JHU-58 is promising for research of neuropathic pain.

JAX-77 is a potent root architecture modulator. JAX-77 maintains primary root length while substantially increasing lateral root numbers, thereby optimizing the plant’s overall root system. JAX-77 is the key intermediate metabolite formed from the hydrolysis of JAX-44 and can be converted to Indole-3-butyric acid (IBA). JAX-77 can be used for auxin biology and root development research.

JAK3-IN-20 is a selective and orally active JAK3 inhibitor with an IC50 of 0.7473 nM. JAK3-IN-20 forms a covalent bond with JAK3 Cys909, outcompetes ATP for catalytic site binding, and blocks JAK-STAT pathway activation. JAK3-IN-20 inhibits migration, proliferation, and tumor growth of Bortezomib-resistant cancer cells. JAK3-IN-20 induces dose-dependent apoptosis. JAK3-IN-20 can be used for the research of Bortezomib-resistant multiple myeloma.

JAK3-IN-19 (Compound 4) is a JAK3 inhibitor. JAK3-IN-19 can be used for cancer research.

JAK2-IN-20 is an orally active dual inhibitor targeting JAK2 kinase (IC50=49.17 nM) and influenza A virus PB2 protein (IC50=3.337 μM, Kd=2.82 μM). JAK2-IN-20 effectively blocks the JAK/STAT signaling pathway by reducing the phosphorylation levels of STAT1 and STAT3, thereby inhibiting viral replication and downregulating the expression of viral NP and PB2 proteins. In addition, JAK2-IN-20 significantly inhibits the mRNA expression of key inflammatory cytokines such as IL-6, TNF-α and IFN-β in inflammation and influenza infection models. JAK2-IN-20 serves as an important tool molecule for the study of influenza A virus infection and related pathologies.

JAK2-IN-18 (Compound example1) is a selective JAK2 inhibitor. JAK2-IN-18 can inhibit JAK-STAT signaling and shows an IC50 of <100 nM for pSTAT5 in HEL9217 cells. JAK2-IN-18 can inhibit the proliferation of abnormally proliferating myeloid cells and can be used for the research of myeloproliferative disorders, such as essential thrombocythemia.

JAK2-IN-16 (Compound Example 4) is a JAK2 V617F inhibitor. JAK2-IN-16 can be used for the research of cancer.

JAK2-IN-15 is an orally active, potent, selective JAK2 inhibitor (IC50 = 1.17 nM). JAK2-IN-15 can inhibit the AK2-STAT signaling pathway. JAK2-IN-15 significantly improves key pathological indicators such as hematocrit and splenomegaly in an Epoetin beta (rhEPO)-induced mouse model. JAK2-IN-15 can be used for the study of Polycythemia Vera (PV).

JAK1-IN-20 (Compound 38) is a gut-restricted, orally active, selective JAK1 inhibitor with an IC50 of <0.5 nM. JAK1-IN-20 inhibits the enzymatic activity of JAK1, reduces the production of proinflammatory cytokines (TNF-α, IL-6), and suppresses the phosphorylation of STAT3. JAK1-IN-20 ameliorates ulcerative colitis. JAK1-IN-20 can be used for the research of inflammatory bowel disease.

JAK1/2-IN-2 (Compound 37) is a potent and selective JAK1/2 inhibitor with Ki values of 2 and 0.6 nM .

JAK1/2 ligand 1 is the ligand of JAK1/2 and can be used for the synthesis of PROTACs, such as JAK1/2 Ligand-Linker Conjugates 1.

J-104118 is a potent and orally active squalene synthase (SQS) inhibitor with an IC50 of 0.52 nM. J-104118 inhibits cholesterol synthesis in mice. J-104118 can be used for cholesterol-lowering research.

IVL 745 (XRP 1745A) is a very late antigen 4 (VLA-4, integrin α4β1) antagonist. IVL 745 reduces the airway inflammatory response of sensitized rats and sheep. IVL 745 can be used for airway inflammation and asthma research.

iVeliparib-AP6 is a proteolysis-targeting chimera (PROTAC) molecule designed based on Veliparib, which targets PARP1/2. The DC50s of iVeliparib-AP6 for inducing the degradation of PARP1 and PARP2 are 36 nM and 63 nM, respectively, and its IC50s are 69 nM and 21 nM, respectively. iVeliparib-AP6 contains a Veliparib-based PARP inhibitor warhead linked to a CRBN E3 ligase binder; it uses Thalidomide as a ligand to recruit CRBN E3 ubiquitin ligase and exerts the PARP2 degradation mechanism.

ITRI-90 is an orally active androgen receptor (AR) PROTAC degrader. ITRI-90 effectively degrades both full-length AR (AR-FL) and the splice variant AR-V7 protein via the ubiquitin-proteasome system, thereby inhibiting AR transcriptional activity and the target gene expression. ITRI-90 significantly inhibits the proliferation of prostate cancer cells and induces apoptosis, include Enzalutamide-resistant growth cell. ITRI-90 exhibits favorable pharmacokinetic properties and demonstrates potent antitumor efficacy in vivo. ITRI-90 can be used for prostate cancer research.

ITA-5 is a TBK1 inhibitor based on the structure of itaconic acid. can significantly inhibit the secretion of IFN-β. ITA-5 can inhibit the phosphorylation of TBK1, IRF3, and STAT1. ITA-5 can be used for research on autoimmune diseases and excessive inflammation.

ISR activator 3 (Compound cc81) is the active metabolite of A8. ISR activator 3 activates the integrated stress response (ISR) by binding to RIG-I (KD ≈ 0.55 μM), without inducing lipid droplet clearance. ISR activator 3 enhances the interferon response under viral mimicry signals. ISR activator 3 can be used for research on neurodegenerative diseases and immune stress.

Isofusidienol A (Compound 26) is a chromone compound. Isofusidienol A can be isolated from Artemisia vulgaris. Isofusidienol A has significant antibacterial activity against Bacillus subtilis. Isofusidienol A also has potent antifungal activity against Candida albicans. Isofusidienol A can be used for bacterial and fungal infections research.

ISA 27 is a small-molecule MDM2-p53 protein-protein interaction inhibitor. ISA 27 inhibits MDM2-mediated p53 ubiquitination and degradation. ISA 27 is promising for research of p53-mutant solid tumors (e.g., thyroid, breast cancer).

IRBM-Z-2 is a non-competitive, orally active Zika virus (ZIKV) NS2B-NS3 protease inhibitor, with IC50 values of 0.04 μM and 3.1 μM against the wild-type and I156T mutant strains, respectively. IRBM-Z-2 exhibits broad-spectrum anti-flavivirus potential, with IC50 values of 2.1 μM and 0.09 μM against the NS2B-NS3 proteases of dengue virus 2 (DENV2) and West Nile virus (WNV), respectively. IRBM-Z-1 inhibits ZIKV replication and alleviates virus-induced cytopathic effects. IRBM-Z-1 can be used in studies related to ZIKV infection.