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Catalog No.
Product Name
Application
Product Information
Citations
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CDK2 inhibitor
INX-315 is an orally active and selective CDK2 inhibitor that induces G1 phase cell cycle arrest by reducing phosphorylation of CDK2 substrates. It exhibits dose-dependent tumor growth inhibition in xenograft mouse models and holds promise as a therapeutic candidate for cancer research targeting CDK2-driven malignancies. -
CDK8/19 inhibitor
Senexin B (SNX2-1-165; BCD-115) is a potent, highly water-soluble, and orally bioavailable inhibitor of CDK8 and CDK19, with Kd values of 140 nM for CDK8 and 80 nM for CDK19. It is a valuable tool for studying transcriptional regulation and has potential applications in cancer and inflammatory disease research. -
CDK2 inhibitor
Cirtociclib (BLU-222) is an orally active and highly selective CDK2 inhibitor. It disrupts retinoblastoma (Rb) signaling, leading to G1 cell cycle arrest and apoptosis, particularly in CCNE1-amplified endometrial cancer cells. Cirtociclib is a promising candidate for targeted therapy in CDK2-driven malignancies. -
CDK Inhibitor
Inixaciclib is a potent cyclin-dependent kinase (CDK) inhibitor with potential applications in anticancer research. By targeting CDKs involved in cell cycle regulation, Inixaciclib can inhibit tumor cell proliferation and is being explored as a therapeutic candidate in cancer treatment. -
CDK2 inhibitor
AZD8421 is a selective CDK2 inhibitor with an IC50 of 9 nM and demonstrated selectivity over CDK1, CDK4, and CDK6. It inhibits cancer cell proliferation by blocking pRB phosphorylation, leading to cell cycle arrest and senescence. AZD8421 shows strong single-agent efficacy and synergistic effects when combined with CDK4/6 inhibitors such as Palbociclib in in vivo models of breast and ovarian cancer. Additionally, it exhibits potent activity against drug-resistant breast cancer cells, making it a promising candidate for overcoming resistance in cancer therapy. -
DK/PI3K/BRD4 Inhibitor
SRX3177 is a potent triple inhibitor targeting CDK4/6, PI3K, and BRD4, with IC50 values of <2.5 nM for CDK4, 3.3 nM for CDK6, 79 nM for PI3Kα, 83 nM for PI3Kδ, 3.18 μM for PI3Kγ, and 33 nM and 89 nM for BRD4 BD1 and BD2, respectively. It exhibits broad cytotoxic activity against cancer cells while sparing normal epithelial cells, highlighting its potential as a targeted cancer therapeutic with reduced toxicity. -
RAS inhibitor
ADT-007 is a potent and orally active pan-RAS inhibitor with strong anticancer activity. It binds to RAS in its nucleotide-free conformation, effectively blocking GTP loading and activation. ADT-007 selectively inhibits the proliferation of cancer cells harboring mutated or hyperactivated wild-type RAS isozymes, making it a promising candidate for RAS-driven cancer research and therapy. -
KRAS G12C inhibitor
Fulzerasib (GFH925) is an irreversible inhibitor of KRAS^G12C, demonstrating potent anticancer activity. It exhibits synergistic effects when combined with cetuximab, enhancing the therapeutic efficacy against KRAS^G12C-driven tumors. -
SOS1 inhibitor
RGT-018 is a potent, orally active SOS1 inhibitor that exhibits anti-tumor activity by blocking KRAS activation. By disrupting the SOS1–KRAS interaction, RGT-018 effectively inhibits cancer cell proliferation, making it a promising candidate for targeting KRAS-driven malignancies. -
KRAS G12C inhibitor 36
Glecirasib (Compound 1-2; JAB-21822) is a potent and orally active inhibitor of KRAS^G12C. As a member of the Ras protein family—key regulators of intracellular signaling involved in cell growth and development—KRAS^G12C is a critical oncogenic driver. Glecirasib shows strong potential for the study and treatment of KRAS^G12C-mediated cancers. -
KRAS G12D inhibitor
Zoldonrasib (RMC-9805) is a potent, orally active inhibitor selectively targeting KRAS^G12D. It induces apoptosis in KRAS^G12D-mutant cancer cells and holds significant potential for the study and treatment of KRAS^G12D-driven malignancies. -
KRAS G12C inhibitor
Olomorasib is a potent and selective inhibitor of KRAS^G12C, demonstrating significant tumor growth inhibition, as reported in patent WO2021118877A1. It is under investigation for targeted therapy in KRAS^G12C-mutant cancers -
FLT3/CHK2 inhibitor
Lasmotinib (PHI-101) is a dual inhibitor of FLT3 and CHK2 with potent activity against FLT3 single activating mutations (ITD or TKD), as well as double (ITD/D835Y or ITD/F691L) and triple (ITD/D835Y/F691L) resistance mutations. It synergizes with Venetoclax or Azacytidine to enhance anti-leukemic effects and also demonstrates anticancer activity in ovarian and breast cancer models. -
KRASG12C inhibitor
RMC-4998 is an orally active inhibitor that selectively targets the active, GTP-bound state of the KRAS^G12C mutant. It forms a ternary complex with intracellular cyclophilin A (CYPA) and activated KRAS^G12C, exhibiting an IC50 of 28 nM. RMC-4998 suppresses ERK signaling and induces apoptosis in KRAS^G12C-mutant cancer cells, making it a valuable candidate for tumor research. -
Aurora A/B inhibitor
Tinengotinib (TT00420) is an orally bioavailable, spectrally selective small-molecule kinase inhibitor targeting Aurora A/B (IC50=1.2–3.3 nM), FGFR1/2/3 (IC50=1.5–3.5 nM), VEGFRs, JAK1/2, and CSF1R. It disrupts Aurora kinase-mediated cell cycle progression, inducing G2/M arrest, inhibits the FGFR/JNK-JUN signaling pathway, and activates the MEK/ERK-dependent apoptotic pathway. Tinengotinib exhibits potent anti-tumor proliferation, pro-apoptotic, anti-angiogenic, and tumor microenvironment-modulating activities. It is a promising candidate for research in triple-negative breast cancer (TNBC), gallbladder cancer, and tumor immune microenvironment studies. -
RAS inhibitor
RMC-7977 is an orally bioavailable, triple-complex RAS inhibitor that functions by simultaneously binding to cyclophilin A (CypA; K_d = 195 nM) and KRAS^G12V (K_d = 292 μM), facilitating the formation of a stable inhibitory complex. It exhibits broad-spectrum activity against RAS isoforms—including KRAS, NRAS, and HRAS—across both wild-type and mutant variants. RMC-7977 suppresses key oncogenic signaling pathways by inhibiting the phosphorylation of ERK, CRAF, and RSK, while promoting apoptosis through enhanced PARP cleavage. This dual mechanism results in significant tumor regression and reduced acquired resistance in KRAS^G12C-driven cancer models. It also shows favorable tolerability across a range of RAS-mutant tumor models, positioning it as a promising therapeutic candidate for RAS-driven malignancies. -
KRAS-G12C(ON) Inhibitor
Elironrasib is an orally active, covalent inhibitor specifically targeting the active GTP-bound form of KRAS^G12C (KRAS^G12C(ON)). It uniquely functions by forming a stable tri-complex with KRAS^G12C(ON) and cyclophilin A (CypA) within tumor cells, leading to steric hindrance that blocks the interaction between KRAS and its downstream effectors. This mechanism effectively suppresses RAS-mediated signaling, particularly the ERK pathway. Elironrasib induces apoptosis in KRAS^G12C-mutant H358 non-small cell lung cancer cells and demonstrates potent antiproliferative activity across KRAS^G12C-mutant cell lines, with a median IC₅₀ of 0.11 nM. Its high specificity and novel mechanism make it a promising therapeutic candidate for cancers driven by KRAS^G12C mutations. -
KRAS/ERK/RAS Inhibitor
LUNA18 is an orally bioavailable cyclic peptide that functions as a dual inhibitor of KRAS and ERK signaling pathways. It disrupts the interaction between RAS and guanine nucleotide exchange factors (GEFs), effectively inhibiting RAS activation and downstream signaling. In RAS-mutated cancer cells, LUNA18 reduces cell proliferation while modulating key signaling nodes, including phosphorylation of ERK and AKT. In preclinical studies, LUNA18 demonstrates potent anticancer activity, particularly in xenograft models, by blocking RAS-driven tumor growth. It shows significant cellular efficacy against cancer cell lines harboring KRAS mutations, including colon, gastric, pancreatic, and non-small cell lung cancers, highlighting its therapeutic potential as a targeted agent for RAS-driven malignancies. -
Aurora B inhibitor
SP-96 is a highly potent, selective, and non-ATP-competitive inhibitor of Aurora B kinase, with an IC₅₀ of 0.316 nM. It exhibits exceptional selectivity, showing over 2000-fold greater specificity for Aurora B compared to off-target kinases such as FLT3 and KIT. In NCI-60 cancer cell line screening, SP-96 demonstrates selective antiproliferative activity, notably against the triple-negative breast cancer (TNBC) cell line MDA-MB-468 (GI₅₀ = 107 nM). SP-96 is a valuable tool for investigating Aurora B–driven oncogenic pathways and holds promise for the development of targeted therapies in TNBC and other malignancies. -
Aurora A inhibitor
CD532 is a potent Aurora A kinase (AURKA) inhibitor with an IC₅₀ of 45 nM. It exerts a dual mechanism of action by both inhibiting AURKA enzymatic activity and promoting the degradation of the MYCN oncoprotein. CD532 directly binds to AURKA and induces a global conformational shift, disrupting its functional interactions. This unique mode of action makes CD532 a valuable tool for cancer research, particularly in MYCN-amplified tumors such as neuroblastoma. -
Multi-target Inhibitor
Chiauranib (CS2164) is an orally active, multi-targeted small molecule inhibitor with potent anticancer activity. It targets key kinases involved in tumor angiogenesis, including VEGFR1, VEGFR2, VEGFR3, PDGFRα, and c-Kit, as well as mitosis-related kinase Aurora B and inflammation-associated kinase CSF-1R. Chiauranib exhibits IC₅₀ values ranging from 1 to 9 nM against these targets. Through simultaneous inhibition of angiogenesis, cell division, and inflammation pathways, Chiauranib exerts strong antitumor effects and is a promising candidate for the treatment of various solid tumors. -
Aurora A inhibitor
JAB-2485 is a highly potent and selective inhibitor of Aurora kinase A (AURKA), with an IC₅₀ of 0.33 nM. It exhibits exceptional selectivity, showing approximately 1700-fold preference for AURKA over Aurora kinase B (AURKB). JAB-2485 induces cell cycle arrest and apoptosis, making it a promising candidate for cancer research, particularly in tumors driven by dysregulated mitotic signaling. -
Aurora A inhibitor
Aurkin A is an allosteric inhibitor that disrupts the interaction between Aurora A kinase (AURKA) and its co-activator TPX2 by selectively targeting the TPX2 binding site on Aurora A. It binds with a dissociation constant (K\_d) of 3.77 μM, thereby interfering with Aurora A activation and its downstream mitotic functions. Aurkin A offers a unique mechanism of action compared to ATP-competitive inhibitors and serves as a valuable tool for studying Aurora A–TPX2–mediated signaling in cell division and cancer progression. -
Aurora A-TPX2 interaction inhibitor
CAM2602 is a selective inhibitor targeting the interaction between Aurora A kinase and its co-activator TPX2, with a high binding affinity of 19 nM for Aurora A. It effectively inhibits the growth of pancreatic cancer cells and demonstrates antitumor activity in solid tumor transplant models. Mechanistically, CAM2602 increases the proportion of phospho-histone H3 (PH3) positive cells—indicative of mitotic arrest—while decreasing the levels of Aurora A phosphorylated at threonine 288 (P-Thr288), a marker of Aurora A activation. These effects collectively contribute to its ability to disrupt mitosis and suppress tumor progression. -
Aurora kinase inhibitor
DBPR728 is an acyl prodrug of 6K465, engineered to improve pharmacokinetic properties by reducing the number of hydrogen bond donors, thereby enhancing membrane permeability and stability. As a prodrug of 6K465, DBPR728 functions as an Aurora kinase inhibitor that destabilizes MYC family oncoproteins, including c-MYC and N-MYC. It exhibits potent antitumor activity, particularly in cancers characterized by MYC overexpression. Notably, DBPR728 offers a 10-fold increase in oral bioavailability compared to 6K465, making it a promising candidate for the development of orally administered therapies targeting MYC-driven malignancies. -
Aurora Kinase A/JAK2 Inhibitor
AJI-214 is a dual-target inhibitor that simultaneously inhibits Aurora kinase A and Janus kinase 2 (JAK2). It directly blocks Aurora A activity, disrupting T cell mitotic progression and polarity, while also inhibiting JAK2-mediated STAT3 phosphorylation, thereby suppressing the differentiation of pro-inflammatory TH1 and TH17 cells. AJI-214 holds therapeutic potential for modulating immune responses and is being investigated for the prevention and treatment of graft-versus-host disease (GVHD). -
Aurora A inhibitor.
6K465 is a pyrimidine-based small molecule inhibitor selectively targeting Aurora A kinase (AURKA). By inhibiting AURKA activity, 6K465 effectively reduces the expression levels of the oncogenic transcription factors c-MYC and N-MYC, contributing to its anticancer effects. This compound shows promise as a therapeutic agent for MYC-driven cancers by disrupting mitotic regulation and oncogene stabilization. -
Aurora kinase inhibitor
Derrone is a prenylated isoflavone that functions as an Aurora kinase inhibitor, exhibiting IC₅₀ values of 6 μM for Aurora B and 22.3 μM for Aurora A. By targeting these key mitotic kinases, Derrone disrupts cell cycle progression and displays notable antitumor activity, making it a promising compound for cancer research focused on mitotic regulation. -
Casein Kinase inhibitor
BTX-A51 (Casein Kinase Inhibitor A51) is a potent, orally bioavailable inhibitor of casein kinase 1α (CK1α). It effectively induces apoptosis in leukemia cells and demonstrates strong anti-leukemic activity in preclinical models, making it a promising therapeutic candidate for hematologic malignancies. -
PI3K/Akt/Ras/Raf/MAPK Inhibitor
Erufosine is a potent inhibitor of the PI3K/Akt and Ras/Raf/MAPK signaling pathways. It demonstrates significant cytotoxic activity against breast cancer cell lines, specifically MCF-7 and MDA-MB-231, with IC50 values of 40.95 μM and 40.8 μM, respectively. By reducing the phosphorylation levels of PI3K (p85), Akt (PKB), and cRaf, Erufosine serves as a valuable tool in the research of breast cancer and myeloid leukemia. -
CDK1 Inhibitor
Albanol B is a selective inhibitor of Cyclin-dependent kinase 1 (CDK1), derived from arylbenzofuran. This compound demonstrates significant potential in cancer research by inhibiting cell proliferation and down-regulating CDK1 expression, leading to G2/M cell cycle arrest and apoptosis in cancer cells. Additionally, Albanol B exhibits anti-Alzheimer's activity, antibacterial properties, and antioxidant effects, while also inducing mitochondrial reactive oxygen species (ROS) production and enhancing phosphorylation levels of AKT and ERK1/2. -
pan-KRAS Inhibitor
pan-KRAS-IN-5 is a pan-KRAS inhibitor that functions by targeting 5′-UTR RNA G-quadruplexes (rG4s). It effectively binds to and stabilizes KRAS rG4s, leading to the inhibition of KRAS translation and downstream signaling via the MAPK and PI3K-AKT pathways. This compound has been shown to induce cell cycle arrest and promote apoptosis in KRAS-driven cancer cells, while also inhibiting tumor growth and KRAS expression in KRAS-mutant xenograft models. pan-KRAS-IN-5 is suitable for investigations into KRAS-related oncogenesis and therapeutic strategies for KRAS-driven cancers. -
HDACs/CDKs Dual Inhibitor
CDK/HDAC-IN-3 is a dual inhibitor targeting histone deacetylases (HDACs) and cyclin-dependent kinases (CDKs). It exhibits potent and selective activity, with IC50 values of 98.32 nM, 98.85 nM, 100 nM, 62.12 nM, 93.28 nM, and 82.87 nM against CDK9, CDK12, CDK13, HDAC1, HDAC2, and HDAC3, respectively. This compound is particularly relevant for research in acute myeloid leukemia (AML), providing insights into therapeutic strategies for this disease. -
Aurora-A Inhibitor
PHA-680626 is a selective inhibitor of Aurora-A kinase, disrupting its interaction with N-Myc. This compound effectively inhibits the kinase activities of both AURKA and Bcr-Abl, leading to the degradation of N-Myc. Additionally, PHA-680626 reduces phosphorylation levels of CrkL and histone H3. Its anti-proliferative and pro-apoptotic effects have been demonstrated in Imatinib-resistant chronic myeloid leukemia cell lines and primary CD34+ hematopoietic stem cells, making it a valuable tool for research in cancer therapeutics. -
CDK Inhibitor
Ryuvidine is a selective inhibitor of cyclin-dependent kinases (CDKs), specifically targeting SET domain-containing protein 8 (SETD8) with an IC50 of 0.5 µM, thereby suppressing the monomethylation of histone H4 at lysine 20 (H4K20). Additionally, Ryuvidine inhibits CDK4 with an IC50 of 6.0 µM and KDM5A, leading to the blockade of DNA synthesis. Its biological activity includes anticancer effects against various tumor types, including breast cancer, and it also demonstrates potential therapeutic benefits in arthritis research. -
CDK9/EZH2 Dual-target Inhibitor
CDK9/EZH2-IN-1 is a dual-target inhibitor designed to inhibit both CDK9 and EZH2, exhibiting IC50 values of 83.9 nM and 108.6 nM, respectively. This compound demonstrates significant biological activity by inducing apoptosis and causing DNA double-strand breaks (DSBs). It effectively inhibits the proliferation of various cancer cell lines, including MKN45, MDA-MB-453, and SW620, with IC50 values of 136.3 nM, 171.3 nM, and 315.7 nM, respectively. CDK9/EZH2-IN-1 is suitable for research applications in understanding cancer cell biology and therapeutic development. -
PLK1 PBD Inhibitor
MCC1019 is a selective inhibitor of the Polo-like kinase 1 (PLK1) phosphopeptide-binding domain (PBD), exhibiting an IC50 of 16.4 μmol/L. This compound effectively inactivates the AKT signaling pathway in cancer cells, leading to the induction of apoptosis, necroptosis, and autophagy. MCC1019 demonstrates significant anticancer activity against lung and prostate cancer, making it a valuable tool for cancer research and therapeutic studies. -
CDK6/9 Inhibitor
CDK6/9-IN-2 is a potent dual inhibitor of cyclin-dependent kinases CDK6 and CDK9, with reported IC50 values of 15 nM and 22 nM, respectively. This compound exhibits selectivity for CDK2, CDK8, and CDK11. CDK6/9-IN-2 effectively inhibits the proliferation of HaCaT cells stimulated by IFN-γ and TNF-α, while also suppressing the STAT3 signaling pathway and the expression of inflammatory factors. Its ability to alleviate psoriatic dermatitis makes CDK6/9-IN-2 valuable for research in psoriasis and related inflammatory conditions. -
KRAS Inhibitor
BBO-11818 is a highly selective non-covalent pan-KRAS inhibitor, targeting the Switch-II/Helix 3 pocket with an IC50 range of 28-120 nM. This compound effectively disrupts the KRAS:RAF1 interaction, leading to inhibition of the MAPK signaling pathway, resulting in significant anti-tumor effects. It demonstrates the ability to not only inhibit cell proliferation and induce apoptosis but also promote tumor regression in xenograft models. BBO-11818 is particularly valuable in research focused on KRAS mutation-related malignancies, including pancreatic cancer, non-small cell lung cancer, and colorectal cancer, and exhibits synergistic effects when used in combination with other therapeutic agents. -
CDK Inhibitor
AS2863619 free base is a selective inhibitor of cyclin-dependent kinases 8 and 19 (CDK8 and CDK19), demonstrating IC50 values of 0.61 nM and 4.28 nM, respectively. This compound drives the conversion of antigen-specific effector and memory T cells into Foxp3+ regulatory T (Treg) cells, thereby offering potential therapeutic approaches for various immunological conditions. The inhibition of CDK8/19 by AS2863619 enhances STAT5 activation, leading to the upregulation of the Foxp3 gene and promoting Treg cell development. -
CDK3 Inhibitor
Vanicoside B is a potent inhibitor of cyclin-dependent kinase 8 (CDK8), derived from the herb Persicaria dissitiflora. This compound demonstrates significant anti-tumor activity by disrupting CDK8-mediated signaling pathways and reducing the levels of proteins associated with epithelial-mesenchymal transition. As a result, Vanicoside B induces cell cycle arrest and apoptosis, making it a valuable reagent for cancer research and therapeutic investigations targeting CDK8 pathways. -
ROCK2 Inhibitor
ROCK2-IN-12 is a selective ROCK2 inhibitor, demonstrating an IC50 of 7.0 nM for ROCK2 relative to ROCK1. This compound exhibits potent antifibrotic effects by modulating the TGF-β/Smad and ROCK2/STAT3 signaling pathways, effectively reducing collagen deposition and reversing fibrosis in Bleomycin-induced pulmonary fibrosis mouse models. ROCK2-IN-12 is suitable for investigating lung diseases, particularly pulmonary fibrosis. -
ROCK2 Inhibitor
ROCK2-IN-7 is a selective inhibitor of the Rho-associated protein kinase 2 (ROCK2). It effectively disrupts ROCK2/pSTAT3 signaling pathways, leading to decreased systemic immune activation and reduced inflammation. This compound is particularly valuable in studies related to autoimmune conditions, such as psoriasis, as it provides insights into the modulation of immune responses and inflammatory processes. -
CDK8/19 Inhibitor
CDK8/19-IN-2 is a potent and orally active inhibitor of cyclin-dependent kinases 8 and 19, exhibiting IC50 values of 2.08 nM and 2.49 nM, respectively. This compound is crucial for research focusing on acute myeloid leukemia (AML), breast cancer, and lymphoma, where inhibition of CDK8 and CDK19 can influence tumor proliferation and survival. Its selectivity and efficacy make it a valuable tool in studying the role of these kinases in various oncogenic pathways. -
PLK Inhibitor
Poloxipan is a pan-specific inhibitor targeting polo-like kinases (PLKs), specifically interfering with the Polo-box domain at the C-terminus. It demonstrates IC50 values of 3.2 μM, 1.7 μM, and 3.0 μM against PLK-1, PLK-2, and PLK-3, respectively. Additionally, Poloxipan inhibits various phospho-tyrosine binding domains, including the forkhead-associated domain of CHK-2 and the WW domain of peptidyl-prolyl cis/trans isomerase (PIN1). This compound is valuable for applications in cancer research, particularly in studies involving PLK pathways and associated cellular processes. -
CDK8/19 Inhibitor
CDK8-IN-16 is a potent dual inhibitor of cyclin-dependent kinases 8 and 19, demonstrating IC50 values of 5.1 nM and 5.6 nM, respectively. This compound effectively inhibits phospho-STAT1SER727 with an IC50 of 17.9 nM in SW620 cells and modulates the WNT signaling pathway with an IC50 of 7.2 nM in 7dF3 cells. CDK8-IN-16 exhibits favorable pharmacokinetic properties, including an oral bioavailability of 57% in rat models, making it a valuable tool for research in cancer biology and therapeutic development. -
KRAS G12D Inhibitor
KRAS G12D-IN-30 is a selective inhibitor of the KRAS G12D mutant, targeting the KRAS oncogene involved in various cancers. By inhibiting the activation of the downstream MAPK signaling cascade, specifically the Raf1-MEK-ERK pathway, this compound provides valuable insights into oncogenic signaling mechanisms. KRAS G12D-IN-30 is suitable for cancer research applications, particularly in studies focusing on KRAS-driven tumor biology and therapeutic strategies. -
KRAS Inhibitor
KRAS inhibitor-27 is a specific inhibitor targeting KRAS mutations, particularly effective against KRAS G12D and G12V variants. It demonstrates potent biological activity with IC50 values of 378 nM and 0.6 nM in AsPC-1 and SW620 cell lines, respectively, while showing a markedly reduced effect on wildtype KRAS HT-29 cells (IC50 3230 nM). This compound effectively inhibits ERK phosphorylation and reduces DUSP4 expression, thereby disrupting the MAPK signaling pathway. KRAS inhibitor-27 is valuable for research applications focusing on cancer biology and therapeutic strategies against KRAS-driven tumors. -
CDK2/CDK5 Inhibitor
(S)-PHA533533 is an inhibitor of cyclin-dependent kinases CDK2 and CDK5, demonstrating blood-brain barrier permeability with IC50 values of 37 nM and 55 nM, respectively. This compound effectively restores UBE3A expression by downregulating UBE3A-ATS, thereby alleviating the epigenetic silencing of paternal UBE3A in mature neurons. (S)-PHA533533 is a valuable tool for research applications related to Angelman syndrome and offers insights into therapeutic strategies for this genetic disorder.
