Catalog No.
Product Name
Application
Product Information
Citations
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KRAS G12C inhibitor
Elisrasib (D3S-001) is an orally active KRAS^G12C inhibitor that potently inhibits the proliferation of KRAS^G12C-mutant H358 and MIA PaCa-2 cells, with IC₅₀ values of 0.6 nM and 0.44 nM, respectively. It demonstrates good metabolic stability in hepatocytes, liver microsomes, plasma, and whole blood across multiple species. Elisrasib also exhibits favorable pharmacokinetic properties and significant antitumor efficacy in mouse models. -
SOS1 inhibitor
SOS1-IN-11 is a potent small-molecule inhibitor of SOS1, exhibiting an IC₅₀ value of 30 nM. It is used in research to disrupt the SOS1–KRAS interaction and modulate RAS signaling pathways in cancer models. -
Rho/MRTF/SRF Inhibitor
CCG-232601 (compound 8f) is a potent and orally active inhibitor of the Rho/MRTF/SRF transcriptional pathway. It effectively inhibits the development of bleomycin-induced dermal fibrosis in mice and holds potential for antifibrotic research in systemic scleroderma and related fibrotic disorders. - CMC2.24 (TRB-N0224) is an orally active tricarbonylmethane compound that exhibits antitumor activity in pancreatic cancer models by inhibiting Ras activation and downstream ERK1/2 signaling. It is also a potent inhibitor of zinc-dependent matrix metalloproteinases (MMPs), with IC₅₀ values ranging from 2.0 to 69 μM. Additionally, CMC2.24 has therapeutic potential in osteoarthritis, where it restores cartilage homeostasis and reduces chondrocyte apoptosis through modulation of the NF-κB/HIF-2α pathway.
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RAS inhibitor
GDC-6036-NH is a precursor compound described in patent WO2020097537A2 and serves as a key intermediate for the synthesis of Compound 17a/b. Compound 17a/b functions as a RAS inhibitor and is suitable for use in cancer research, particularly in studies targeting RAS-driven signaling pathways. -
KRAS G12C inhibitor
AZD4625 (Compound 21) is a highly potent, selective, covalent, and allosteric inhibitor of the mutant GTPase KRAS^G12C. It exhibits strong target engagement and high oral bioavailability, making it a promising candidate for the treatment of KRAS^G12C-driven cancers. -
KRAS G12D inhibitor
HRS-4642 is a selective KRAS^G12D inhibitor with a dissociation constant (Kd) of 0.083 nM, demonstrating potent anti-cancer activity. It synergizes with Carfilzomib and exhibits strong in vivo efficacy, promoting remodeling of the tumor microenvironment into an immune-activating state.
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RAS(ON) Inhibitor
Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS(ON) inhibitor that disrupts the interaction between wild-type or mutant RAS proteins and the RAS-binding domain of BRAF. It exhibits EC₅₀ values ranging from 28 to 220 nM across wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. RMC-6236 inhibits pERK signaling and demonstrates anti-tumor activity in KRAS-mutant tumor models.
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pan-KRAS Inhibitor
BI-2865 is a non-covalent pan-KRAS inhibitor that binds to wild-type and mutant KRAS variants, including G12C, G12D, G12V, and G13D, with dissociation constants (K\_D) of 6.9, 4.5, 32, 26, and 4.3 nM, respectively. It inhibits the proliferation of Ba/F3 cells expressing KRAS^G12C, KRAS^G12D, or KRAS^G12V, with a mean IC₅₀ of approximately 140 nM. -
pan-KRAS inhibitor
AMG410 is a non-covalent, selective pan-KRAS inhibitor with IC₅₀ values of 1–4 nM against KRAS^G12D, KRAS^G12V, and KRAS^G13D. It demonstrates over 100-fold selectivity against HRAS and NRAS. AMG410 functions as a dual-state inhibitor, binding both GDP-bound (K\_d = 1 nM) and GTP-bound (K\_d = 22 nM) KRAS, effectively blocking signaling independent of the nucleotide state. It also inhibits proliferation in wild-type KRAS-amplified tumor cells and is suitable for research in colorectal, pancreatic, and lung cancers. -
KRAS G12C inhibitor
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS^G12C inhibitor with an IC₅₀ of <0.01 μM. It covalently binds to the switch II (SW-II) pocket of KRAS^G12C, irreversibly locking the protein in its inactive GDP-bound conformation. -
KRAS Switch I/II Pocket Inhibitor
BI-2852 is a KRAS inhibitor designed to target the switch I/II (SI/II) pocket with nanomolar affinity. Unlike covalent KRAS^G12C inhibitors that bind the switch II pocket, BI-2852 exhibits a distinct mechanism of action and binds preferentially to active KRAS^G12D with \~10-fold greater affinity than KRAS^WT (740 nM vs. 7.5 μM). It disrupts interactions between KRAS and GEFs, GAPs, and effectors, thereby inhibiting downstream signaling and exerting antiproliferative effects in KRAS-mutant cells. -
KRAS G12C inhibitor
Opnurasib (JDQ-443, also known as NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS^G12C inhibitor, as described in patent WO2021120890A1. It exhibits strong antitumor activity in KRAS^G12C-driven cancer models. -
ULK1/2 inhibitor
DCC-3116 is an orally active inhibitor of ULK1/2 that suppresses autophagy in lung cancer cells. By targeting ULK1/2, DCC-3116 inhibits KRAS^G12C-driven signaling pathways, leading to reduced cell proliferation and demonstrating anti-tumor activity in KRAS-mutant lung cancer models. -
TrxR-1 inhibitor
Manumycin A is a polyketide antibiotic that functions as an inhibitor of thioredoxin reductase 1 (TrxR-1). It exhibits anti-tumor activity by inhibiting breast cancer cell growth, potentially through LC3-mediated mechanisms. Manumycin A also downregulates pro-inflammatory cytokine release in TNF-α-stimulated human monocytes, indicating anti-inflammatory potential. Additionally, it inhibits the Ras/Raf/ERK1/2 signaling pathway and hnRNP H1 in castration-resistant prostate cancer cells, thereby suppressing exosome biogenesis and secretion. -
RAS-G12V inhibitor
RMC-5127 is an orally active, brain-penetrant, mutant-selective tri-complex inhibitor targeting RASG12V. It non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages active RASG12V to create a high-affinity tri-complex, thereby sterically blocking RAS-effector interactions. RMC-5127 inhibits RAS signaling in KRASG12V-mutant cancer cells, suppressing proliferation and inducing apoptosis. It holds promise for the study of RAS-mutant cancers, including non-small cell lung cancer. -
KRAS G12D inhibitor
MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor featuring an alkyne-based structure. It binds with high affinity to the switch II pocket of KRAS G12D, with an estimated KD of 0.2 pM, engaging three key substituents that enhance protein interactions. MRTX1133 inhibits SOS1-mediated nucleotide exchange and disrupts formation of the KRAS G12D/GTP/RAF1 complex, thereby blocking downstream mutant KRAS signaling. It selectively targets KRAS G12D mutant cells without affecting KRAS wild-type cells, exhibiting single-digit nanomolar potency in cellular assays and strong antitumor efficacy in KRAS G12D-driven in vivo models. -
ROCK1/2 inhibitor
DJ4 is an ATP-competitive inhibitor of ROCK1/2 and MRCKα/β, with IC₅₀ values of 5 nM and 50 nM for ROCK1 and ROCK2, and 10 nM and 100 nM for MRCKα and MRCKβ, respectively. It blocks stress fiber formation and induces apoptosis, making it a valuable compound for cancer research. -
ROCK 1/2 inhibitor
HSD1590 is a potent inhibitor of Rho-associated protein kinases, with IC₅₀ values of 1.22 nM for ROCK1 and 0.51 nM for ROCK2. It exhibits strong binding affinity to ROCK isoforms (K\_d < 2 nM) and demonstrates low cytotoxicity, making it suitable for further research applications. -
PKC isoenzymes inhibitor
CRT0066854 is a potent and selective inhibitor of atypical protein kinase C (PKC) isoenzymes. It inhibits full-length PKCι, PKCζ, and ROCK-II with IC₅₀ values of 132 nM, 639 nM, and 620 nM, respectively. -
ROCK inhibitor
AS1892802 is a potent, orally active, and highly selective inhibitor of Rho-associated kinase (ROCK). It exhibits a rapid onset of antinociceptive effect, comparable to that of Tramadol and Diclofenac. Unlike traditional analgesics, AS1892802 does not induce gastric irritation or abnormal behavior, making it a promising candidate for research in the treatment of severe osteoarthritis pain. -
ROCK inhibitor
PF-4950834 is a potent, selective, and orally bioavailable ATP-competitive inhibitor of Rho-associated kinases, with IC₅₀ values of 8.35 nM for ROCK2 and 33.12 nM for ROCK1. It effectively inhibits neutrophil migration and is suitable for research on inflammation and immune cell regulation. -
ROCK inhibitor
OXA-06 hydrochloride is an ATP-competitive inhibitor of Rho-associated protein kinase (ROCK) that suppresses anchorage-dependent growth and invasion of non-small cell lung cancer (NSCLC) cell lines. It inhibits cofilin phosphorylation without inducing apoptosis. -
PROTAC Wee1 degrader
Pomalidomide-C3-adavosertib is a rapid and selective PROTAC degrader of Wee1, with an IC₅₀ of 3.58 nM. It exhibits anti-proliferative activity against cancer cells and induces apoptosis. -
Staurosporine Analog
Stauprimide is a staurosporine analog that promotes embryonic stem cell (ESC) differentiation. It selectively binds to the MYC transcriptional regulator NME2, blocking its nuclear localization in ESCs and thereby downregulating MYC transcription. -
Kinases PROTAC/Nek9 Inhibitor
DB0614 is a PROTAC molecule utilizing a cereblon ligand, designed as a selective and potent degrader of NEK9 and other kinases. It induces the degradation of multiple kinases, including ABL1, ABL2, BLK, CDK11B, CDK4, CSK, EPHA3, FER, GAK, LIMK1, MAP3K20, MAP4K1–3, MAP4K5, MAPK14, MAPK7–9, MAPKAPK2/3, NLK, PDIK1L, PTK2B, RIPK1, RPS6KA1/3, SIK2/3, STK35, TNK2, and ULK1. DB0614 is suitable for research involving diseases or disorders driven by aberrant kinase activity. -
CDK inhibitor
(R)-CR8 is a second-generation analog of Roscovitine and a potent inhibitor of CDK1, CDK2, CDK5, CDK7, and CDK9. It inhibits CDK1/cyclin B (IC₅₀ = 0.09 μM), CDK2/cyclin A (0.072 μM), CDK2/cyclin E (0.041 μM), CDK5/p25 (0.11 μM), CDK7/cyclin H (1.1 μM), CDK9/cyclin T (0.18 μM), and CK1δ/ε (0.4 μM). (R)-CR8 induces apoptosis, exhibits neuroprotective effects, and functions as a molecular glue degrader that promotes the degradation of cyclin K. -
CDK12/CDK13 PROTAC degrader
YJ1206 is an orally active and selective PROTAC degrader targeting CDK12 and CDK13, with an IC50 of 12.55 nM in VCaP cells. It induces DNA damage, promotes apoptosis, and leads to tumor regression in orthotopic WA74 patient-derived xenograft (PDX) models of resistant prostate cancer. Additionally, YJ1206 enhances antitumor efficacy when used in combination with AKT pathway inhibitors, highlighting its potential for combination therapy in advanced prostate cancer. -
CDK4/6 inhibitor
Culmerciclib (TQB3616) is a potent cyclin-dependent kinase (CDK)4/6 inhibitor with strong antineoplastic activity. It demonstrates significant synergistic antitumor effects in estrogen receptor (ER)-positive/HER2-negative and HER2-positive breast cancer models when combined with endocrine therapy or HER2-targeted treatments, supporting its potential for combination cancer therapy. -
CDK7 Inhibitor
SY-5609 (CDK7-IN-3) is an orally active, highly selective, and noncovalent inhibitor of CDK7, with a Kd of 0.065 nM. It demonstrates minimal activity against CDK2 (Ki = 2600 nM), CDK9 (Ki = 960 nM), and CDK12 (Ki = 870 nM), confirming its selectivity. SY-5609 induces apoptosis in tumor cells and exhibits potent antitumor activity, making it a promising candidate for targeted cancer therapy. -
CDK5 inhibitor
CP681301 is a potent CDK5 inhibitor with demonstrated antiproliferative activity. It reduces the expression of key stemness and proliferation markers—including CD133, OLIG2, SOX2, KI67, and phosphorylated CDK5—in glioma stem cells (GSCs). CP681301 also impairs self-renewal capacity in mouse glioma xenograft models and exhibits anti-tumor activity in *Drosophila*, making it a promising compound for glioma and cancer stem cell research. -
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.
