CL2A-SN-38, SN-38 (topoisomerase-I inhibitor) derivative, is a peptide linker. CL2A-SN-38 is conjugated to the anti-Trop-2-humanized antibody, SN-38-anti-Trop-2 antibody-drug conjugate (ADC) against several human solid tumor types, provides significant and specific antitumor effects against a range of human solid tumor types[1].
Methyl 2-acetoxybenzoate (Methyl acetylsalicylate) is a safe and simple anti-inflammatory aspirin prodrug. Methyl 2-acetoxybenzoate (Methyl acetylsalicylate) can be chemical or enzymatically hydrolysed to methyl 2-hydroxy benzoate. Methyl 2-acetoxybenzoate (Methyl acetylsalicylate) can be used as analgesic agent in liniments and also inflammatory diseases research[1].
E6446 dihydrochloride is a potent and orally acitve TLR7 and TLR9 antagonist, used in the research of deleterious inflammatory responses.
DW-1350 is a LTB4 receptor antagonist.
IL-17 modulator 2 (compound 159) is an orally active modulator of IL-17. IL-17 modulator 2 significantly reduces IL-6, IFN-γ, and edema. IL-17 modulator 2 can used in study arthritis[1].
CB2 modulator 1 (compound 130) is a potent CB2 modulator. CB2 modulator 1 has the potential for immunedisorders, inflammation, osteoporosis, renal ischemia[1].
GSK 4027 is a chemical probe for the PCAF/GCN5 bromodomain with an pIC50 of 7.4±0.11 for PCAF in a time-resolved fluorescence resonance energy transfer (TR-FRET) assay.
CU-CPT-9a is a specific TLR8 antagonist, with an IC50 of 0.5 nM.
Tolmetin sodium dihydrate is a non-steroidal antiinflammatory agent, and acts as a non-selective COX inhibitor.
Fluasterone is a potent G6PD inhibitor with a Ki of 0.51 μM. Fluasterone has anti-inflammatory, cancer preventive, and anti-diabetic effects. Fluasterone is orally active[1][2][3].
Procaterol hydrochloride hemihydrate is an orally active β2 adrenoreceptor agonist. Procaterol hydrochloride hemihydrate can be used for the research of asthma[1][2][3].
QL9 (QLSPFPFDL) is a high-affinity alloantigen for the 2C T cell receptor (TCR).
Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures[1].Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB[2].Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis[1].Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway[3].
Nebentan potassium (YM598) is a potent, selective and orally active non-peptide endothelin ETA receptor antagonist through the modification of Bosentan (HY-A0013). Nebentan potassium inhibits [125I] endothelin-1 binding to cloned human endothelin ETA and ETB receptor, with Ki of 0.697 nM and 569 nM, respectively[1]. YM598 can ameliorate the progression of cor pulmonale and myocardial infarction in vivo[2].
Communic acid ((+)-Communic acid) is a natural compound isolated from the branches of Platycladus orientalis. Communic acid displays minimum inhibitory concentration of 31 μM and IC50 of 15 μM against M. tuberculosis H37Ra.Communic acid exhibits protective effects against UVB-induced skin aging[1][2][3].
Human PD-L1 inhibitor III is a human PD-L1 inhibitor.
Etimumotide is an immunological agent for active immunization, as well as an antineoplastic agent[1].
Broussonin C is a competitive inhibitor of Tyrosinase that can be isolated from Broussonetia kazinoki. Broussonin C inhibits monophenolase and diphenolase with IC50s of 0.43 and 0.57 μM, respectively[1].
CC-99677 is a potent, covalent, and irreversible inhibitor of the mitogen-activated protein (MAP) kinase-activated protein kinase-2 (MK2) pathway in both biochemical (IC50=156.3 nM) and cell based assays (EC50=89 nM). CC-99677 is extracted from patent WO2020236636, compound 1[1].
[Lys5,MeLeu9,Nle10]-NKA(4-10) is a highly selective and potent NK2 receptor agonist, with an IC50 of 6.1 nM[1].
BI-2545 is a novel potent, selective, orally available Autotaxin inhibitor with IC50 of 2.1 and 3.4 nM for huamn and rat ATX, respectively; displays good potency in the LPA and rat whole blood assay (IC50=29 nM); shows substantial lowering of LPA in vivo, and excellent PK/Target Engagement relationship.
Fexofenadine-d10 (hydrochloride) is deuterium labeled Fexofenadine (hydrochloride). Fexofenadine hydrochloride (MDL-16455 hydrochloride), a H1R antagonist, is an anti-allergic agent used in seasonal allergic rhinitis and chronic idiopathic urticarial (person aged ≥16 years)[1].
Ethacrynic acid is a diuretic. Ethacrynic acid is an inhibitor of glutathione S-transferases (GSTs). Ethacrynic acid is a potent inhibitor of NF-kB-signaling pathway, and also modulates leukotriene formation. Ethacrynic acid also inhibits L-type voltage-dependent and store-operated calcium channel, leading to relaxation of airway smooth muscle (ASM) cells. Ethacrynic acid has anti-inflammatory properties that reduces the retinoid-induced ear edema in mice[1][2][3][4].
Murlentamab (3C23K; GM102) is a humanized anti-AMHRII antibody. AMHRII is the anti-Müllerian hormone receptor. Murlentama significantly promotes macrophage-mediated antibody-dependent cell-mediated cytotoxicity (ADCC). Murlentama stimulates pro-inflammatory and anti-tumor internal environment, recruits and activates T cells. Murlentama suppresses tumors growth by inducing naïve macrophage orientation and promoting tumor-associated macrophage (TAM) reprogramming[1].
APETx2, a sea anemone peptide from Anthopleura elegantissima, is a selective and reversible ASIC3 inhibitor, with an IC50 of 63 nM. APETx2 directly inhibits the ASIC3 channel by acting at its external side. APETx2 could reverses acid‐induced and inflammatory pain[1][2].
PDE4-IN-11 is an inhibitor of phosphodiesterase isoenzyme 4 (PDE4). PDE4-IN-11 displays highly effective bronchodilatory and anti-inflammatory properties, can be used for obstructive or inflammatory airway diseases research[1][2][3].
PNRI-299 is a selective AP-1 transcription inhibitor with IC50 of 20 uM without affecting NF-kappaB transcription (up to 200 uM) or thioredoxin (up to 200 uM).IC50 value: 20 uM [1]Target: AP-1 inhibitorin vitro: PNRI-299 specifically reacts with Ref-1, inhibits AP-1 transcription, and overexpression of the molecular target. Ref-1 attenuates PNRI-299 inhibition of AP-1 transcription. PNRI-299 interacts with the redox nucleophile Cys-65, to aid in the interpretation of structure activity relationships (SARs).in vivo: Treatment with PNRI-299 significantly decreased the influx of eosinophils, monocytes, and macrophages (no significant reduction of lymphocytes was observed) into the lung interstitium and bronchoalveolar lavage fluid, and airway mucus and edema observed in OVA-treated mice.PNRI-299 reduces the pathophysiological responses seen in this murine model of allergic asthma [1]. PNRI-299 had no effects on the inflammatory changes or lethality induced by I/R injury [2].
Psora-4 is a potent and selective inhibitor of Kv1.3 (voltage-gated potassium channels) with an EC50 of 3 nM[1]. Psora-4 has immunosuppressive activity and inhibits proliferation of human and rat myelin-specific effector memory T cells in vitro[2].
Ibudilast(KC-404;AV-411;MN-166) is a relatively nonselective phosphodiesterase inhibitor which has been marketed for treating asthma.Target: PDEIbudilast (3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine) is a nonselective inhibitor of cyclic nucleotide phosphodiesterase (PDE). The inhibition of platelet aggregation and vasodilatation by ibudilast may be due to synergistic elevation of intracellular cyclic nucleotides and release of nitric oxide (NO) or prostacyclin from endothelium, rather than direct inhibition of PDE5 or PDE3. Another important property of ibudilast is its antiinflammatory activity possibly associated with potent inhibition of PDE4. Combined with its relaxing effects on bronchial smooth muscle, antiinflammatory actvity of ibudilast could favorably influence pathophysiology of asthma by antagonizing chemical mediators triggering asthmatic attacks [1, 2]. Ibudilast (AV-411) is a non-selective phosphodiesterase inhibitor that is also known to suppress glial cell activation. Preclinical data indicate that ibudilast crosses the blood-brain barrier, is well tolerated, is active on oral administration, reduces glial activation and attenuates pain symptoms in diverse rat models of neuropathic pain. In addition, it enhances acute morphine analgesia and attenuates morphine tolerance and withdrawal. Thus ibudilast may improve opioid efficacy and is a promising therapeutic candidate for neuropathic pain, with a novel mechanism of action [3].
Pranlukast is a highly potent, selective and competitive antagonist of peptide leukotrienes. Pranlukast inhibits [3H]LTE4, [3H]LTD4, and [3H]LTC4 bindings to lung membranes with Kis of 0.63±0.11, 0.99±0.19, and 5640±680 nM, respectively.