Pyroptosis Inhibitor

BD-AcAc2 (R,S-1,3-Butanediol acetoacetate diester) is an orally active, CNS-penetrant antiepileptic agent. BD-AcAc2 inhibits NF-κB, NLRP3 inflammasome, caspase-1/3, pyroptosis, apoptosis, and enhances autophagy. BD-AcAc2 exhibits antioxidant activity by modulating ROS, MDA, SOD, and GSH levels, and alleviates oxidative stress. BD-AcAc2 mitigates chronic colitis, counteracts Dextran Sodium Sulfate (DSS)-induced pathology, protects against central nervous system oxygen toxicity and acute lung injury, and exhibits anti-seizure efficacy. BD-AcAc2 can be used for the research of colitis, sarcopenia, acute lung injury, seizure, and obesity.

Lenalidomide-¹³C₅,¹⁵N (CC-5013-¹³C₅,¹⁵N) is the ¹³C, ¹⁵N-labeled Lenalidomide (HY-A0003). Lenalidomide (CC-5013) is an orally active immunomodulatory agent that binds CRBN as a molecular glue to alter substrate specificity, inducing ubiquitination and proteasome-dependent degradation of IKZF1, IKZF3 and CK1α. Lenalidomide induces apoptosis by degrading IKZF1/3, and activates p53 by degrading CK1α. Lenalidomide promotes IL-2 release and effector functions of CD8⁺ T/NK cells, while inhibiting TNF-α secretion and M1-type pyroptosis. Lenalidomide can be used in research related to hematological malignancies, acute liver failure and acute kidney injury.

Ac-DmLD-CMK is a caspase 3 inhibitor and a GSDME inhibitor. Ac-DmLD-CMK binds directly to the catalytic domain of caspase-3, blocks caspase-3-mediated cleavage of GSDME, inhibits the activation of caspase 3 and Gsdme in the caspase 3-Gsdme signaling pathway, and reduces the levels of pyroptosis and apoptosis as well as the expression of LDH, IL-6, IL-1β and IL-18. Ac-DmLD-CMK alleviates renal function deterioration, renal tubular epithelial cell injury, inflammatory cytokine secretion, pulmonary structural damage, and chemotherapy-induced nephrotoxicity.

NLRP3-IN-61 (Compound 1) is an inhibitor for NLRP3. NLRP3-IN-61 inhibits pyroptosis in THP-1 cell with an IC₅₀ of 12.6 nM, inhibits IL-β release with an IC₅₀ of 25.3 nM.

ABT-546 (A-216546) is an orally active ET_A receptor antagonist, with K_i values of 0.46 nM and 13000 nM for human ET_A and ET_B receptors, respectively, and exhibits >25000-fold selectivity over the ET_B receptor. ABT-546 effectively inhibits ET-1 (HY-P0202)-induced phosphoinositide hydrolysis (IC₅₀ = 0.59 nM) and arachidonic acid release (IC₅₀ = 3.03 nM), and antagonizes ET-1-induced contraction in isolated vascular rings. ABT-546 crosses the placental barrier but shows extremely low fetal exposure, with a favorable safety profile. ABT-546 inhibits ET-1-induced pressor response and downregulates the NLRP3/ROS/GSDMD-mediated pyroptosis pathway. ABT-546 can be used for research on abdominal aortic aneurysm.

ACT001 (Dimethylaminomicheliolide; DMAMCL) hydrochloride is an orally active, blood-brain barrier-permeable anti-inflammatory and anti-tumor agent. ACT001 hydrochloride exerts microglia-mediated neuroanti-inflammatory effects by inhibiting the AKT/NF-κB/NLRP3 axis and suppressing apoptosis (apoptosis). ACT001 hydrochloride inhibits tumor proliferation by upregulating NKTR and inhibiting AKT. ACT001 hydrochloride alleviates metabolic-associated fatty liver disease by regulating gut microbiota and inhibiting ileal FXR. ACT001 hydrochloride inhibits pyroptosis (pyroptosis) and pro-inflammatory cytokine release by activating PPAR-γ and inhibiting NF-κB/NLRP3.

rac-Lenalidomide-¹³C₅ (CC-5013-¹³C₅) is the ¹³C₅-labeled Lenalidomide (HY-A0003). Lenalidomide (CC-5013) is an orally active immunomodulatory agent that binds CRBN as a molecular glue to alter substrate specificity, inducing ubiquitination and proteasome-dependent degradation of IKZF1, IKZF3 and CK1α. Lenalidomide induces apoptosis by degrading IKZF1/3, and activates p53 by degrading CK1α. Lenalidomide promotes IL-2 release and effector functions of CD8⁺ T/NK cells, while inhibiting TNF-α secretion and M1-type pyroptosis. Lenalidomide can be used in research related to hematological malignancies, acute liver failure and acute kidney injury.

Inclisiran sodium scrambled negative control is the sequence scrambled negative control of Inclisiran sodium.

Lb54 is a caspase-3 and caspase-7 activator with an EC₅₀ of 660.9 nM for human procaspase-3. Lb54 activates caspase-3/7, which cleaves Gasdermin D (GSDMD) at aspartic acid residue 87 to generate a p10 fragment, preventing formation of the pore-forming p30 fragment of GSDMD. Lb54 suppresses GSDMD-mediated pyroptosis through caspase-3/7 activation, thereby attenuating inflammatory responses and conferring protection against sepsis. Lb54 alleviates acute lung injury, and inhibited systemic inflammation by restraining the maturation of monocyte-derived dendritic cells. Lb54 can be used for the research of sepsis.

NLRP3-IN-86 (Compound 8a), a derivative of Songorine (HY-N2080), is a potent and selective NLRP3 inflammasome inhibitor. NLRP3-IN-86 can reduce LPS (HY-D1056)- and Nigericin (HY-127019)-stimulated lactate dehydrogenase (LDH) release (IC₅₀ = 2.69 μM in THP-1 cells and 1.75 μ M in J774A.1 cells). NLRP3-IN-86 can inhibit gasdermin D (GSDMD) cleavage and IL-1β secretion. NLRP3-IN-86 can inhibit cell pyroptosis. NLRP3-IN-86 can be used for research of inflammation.

Morroniside (Standard) is the analytical standard of Morroniside. This product is intended for research and analytical applications. Morroniside has neuroprotective effect by inhibiting neuron apoptosis and MMP2/9 expression.

MNP2 is a NLRP3-ASC interaction inhibitor. MNP2 selectively binds to the PYD domain of ASC (K_a=149 nM) and blocks ASC-PYM binding (K_a=58 nM), thereby inhibiting the interaction between ASC and NLRP3 and suppressing the formation of the NLRP3 inflammasome. MNP2 inhibits IL-1β release and caspase-1 maturation, and reduces the efflux of potassium and chloride ions. MNP2 prevents mitochondrial damage and reactive oxygen species production, and significantly decreases NLRP3 inflammasome formation in neurodegenerative pathologies induced by β-amyloid, Tau protein and α-synuclein. MNP2 is applicable for the research of neurodegenerative diseases.

NLRP3-IN-78 (compound 21) is a NLRP3 inhibitor with the inhibition rate of 46.72% in GSDMD-induced pyroptosis at 5 μM. NLRP3-IN-78 binds to the NLRP3 protein and inhibits GSDMD-NT oligomerization. NLRP3-IN-78 also inhibits GSDMD cleavage, and upstream NF-κB signaling, demonstrating its anti-inflammatory activity.

NLRP3/AIM2-IN-1 is an NLRP3/AIM2 inhibitor with an IC₅₀ of 3.136 μM against NLRP3-dependent pyroptosis. NLRP3/AIM2-IN-1 inhibits IL-1β secretion triggered by NLRP3 inflammasome activation. NLRP3/AIM2-IN-1 exhibits moderate anti-pyroptotic activity. NLRP3/AIM2-IN-1 does not inhibit NLRC4 inflammasome activation. NLRP3/AIM2-IN-1 can be used for studying inflammasome-mediated inflammatory diseases.

NLRP3-IN-62 (Compound 1) is an inhibitor for NLRP3. NLRP3-IN-62 inhibits pyroptosis in THP-1 cell with an IC₅₀ of 0.7 nM, inhibits IL-β release with an IC₅₀ of 108.5 nM.

Ethyl pyruvate (Standard) is the analytical standard of Ethyl pyruvate. This product is intended for research and analytical applications. Ethyl pyruvate is a simple derivative of the endogenous metabolite pyruvate. Ethyl pyruvate is an HMGB1 release inhibitor. Ethyl pyruvate can induce apoptosis by autophagy. Ethyl pyruvate has anti-inflammatory, antioxidant and anti-tumor activity. Ethyl pyruvate can be used in the study of neurodegenerative diseases such as Alzheimer's and Parkinson's disease.

Bisdemethoxycurcumin is an orally effective curcuminoid. Bisdemethoxycurcumin downregulates pro-inflammatory cytokines in macrophages by inhibiting the phosphorylation of PI3K/Akt and p38 MAPK. Bisdemethoxycurcumin relieves autophagy inhibition and promotes lipophagy to clear vascular smooth muscle foam cells by inhibiting the PDK1/Akt/mTOR pathway. Bisdemethoxycurcumin activates the cAMP/Epac/AMPKα axis and the NRF2/HO-1 antioxidant axis, thereby indirectly inhibiting the phosphorylation of NF-κB p65 and pro-inflammatory outputs such as IL-1β/IL-6/TNF-α, so as to alleviate pulmonary oxidative stress, inflammatory infiltration and pulmonary edema. Bisdemethoxycurcumin blocks NLRP3-mediated pyroptosis and protects cartilage extracellular matrix degradation by activating NRF2/HO-1. Bisdemethoxycurcumin also exerts a synergistic effect with potassium iodide against Candida.

ABT-546 (A-216546) hydrochloride is an orally active ET_A receptor antagonist, with K_i values of 0.46 nM and 13000 nM for human ET_A and ET_B receptors, respectively, and exhibits >25000-fold selectivity over the ET_B receptor. ABT-546 hydrochloride effectively inhibits ET-1 (HY-P0202)-induced phosphoinositide hydrolysis (IC₅₀ = 0.59 nM) and arachidonic acid release (IC₅₀ = 3.03 nM), and antagonizes ET-1-induced contraction in isolated vascular rings. ABT-546 hydrochloride crosses the placental barrier but shows extremely low fetal exposure, with a favorable safety profile. ABT-546 hydrochloride inhibits ET-1-induced pressor response and downregulates the NLRP3/ROS/GSDMD-mediated pyroptosis pathway. ABT-546 hydrochloride can be used for research on abdominal aortic aneurysm.

Garlic oil (synthetic) is an orally effective anti-inflammatory, antioxidant, and anticancer agent. Garlic oil (synthetic) inhibits the activation of NF-κB, NFκB2 and NLRP3 inflammasome, and induces the expression of GSTA1, HO-1 and NQO-1. Garlic oil (synthetic) reduces the Bcl-2/Bax protein ratio and activates NNK-induced apoptosis (apoptosis) in lung tissues. Garlic oil (synthetic) attenuates NNK-induced apoptosis in MRC-5 cells and reduces excessive ROS production. Garlic oil (synthetic) alleviates pyroptosis (pyroptosis) and exerts a protective effect against acute lung injury in mice. Garlic oil (synthetic) inhibits lung tumorigenesis in mice and improves small intestinal motility in rats with type 2 diabetes. Garlic oil (synthetic) can be used in research related to acute lung injury, lung cancer, peptic ulcer, type 2 diabetes and hypertension.

NLRP3-IN-26 (compound 15Z) is a NLRP3 inhibitor with the IC₅₀ of 0.13 μM. NLRP3-IN-26 can be used for DSS-induced colitis model study.