JNK-9L (Compound 9l) is a BBB-penetrable and ATP-competitive JNK inhibitor with IC50s of 0.099 and 0.148  μM for JNK1 and JNK3, respectively. JNK-9L significantly inhibits c-jun phosphorylation and Streptozotocin-induced ROS generation with an IC50 of 0.8  nM. JNK-9L can be used for neurodegenerative disorders like Parkinson’s disease research.

(S)-AZD0022 is an isomer of AZD0022, AZD0022 is a selective and orally active KRASG12D inhibitor. AZD0022 inhibits KRAS pathway suppression in the GP2D xenograft model.

SHY-855 is a pan RAS inhibitor. SHY-855 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with IC50 values of 0.3-5 μM. SHY-855 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-855 inhibits the formation of the Ras-GTP activity complex. SHY-855 can be used to the studies of pancreatic cancer and non-small cell lung cancer.

SHY-867 is a pan RAS inhibitor. SHY-867 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with EC50 values of 0.5-3 μM. SHY-867 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-867 inhibits the formation of the Ras-GTP activity complex. SHY-867 can be used to the studies of pancreatic cancer and non-small cell lung cancer.

(R)-KRAS G12D inhibitor 28 hydrochloride dehydrate is the hydrochloride dehydrate of (R)-KRAS G12D inhibitor 28. KRAS G12D inhibitor 28 (Compound 1) is a KRAS G12D inhibitor. KRAS G12D inhibitor 28 (Compound 1) can be used in the cancer research.

VVD-849 is a RAS ligand. VVD-849 binds covalently to cysteine 242 in the RAS binding domain of PI3K p110α and promotes RAS/PI3K interaction. VVD-849 partially inhibits pAKT(S473) in HER2 over-expressing tumors. VVD-849 can be used cancers like breast cancer research.

APS03118 is an orally active, potent and selective rearranged during transfection (RET) inhibitor. APS03118 broadly inhibits RET fusions and mutations (including G810, V804, L730, and Y806 variants), with IC50 values predominantly below 1 nM (0.095 nM for WT; ranging from 0.00438 to 5.72 nM for mutants), and demonstrates marked superiority against RET G810 mutations. APS03118 inhibits the entire RET signaling pathway (including RET, Shc, and ERK1/2), with >20-fold selectivity over most off-target kinases (except FLT3 and YES). APS03118 induces complete tumor regression in KIF5B-RET and CCDC6-RET V804 M patient derived xenografts (PDXs) and significantly prolongs survival in an intracranial CCDC6-RET metastasis mice model. APS03118 can be used for selective RET inhibitor (SRI)-resistant, RET-driven cancer research.

AB19 is a potent Vav1 inhibitor. AB19 inhibits Vav1 and reduces its downstream ERK phosphorylation. AB19 shows anti-proliferative activity in pancreatic cancer models. AB19 can be used for pancreatic cancer research.

BIRB-1017 is a potent inhibitor of p38 MAP kinase. BIRB-1017 can be used in inflammation research.

(±)-Spiro-oxanthromicin A (Compound 4), a polyketide, is a K-Ras inhibitor with an IC50 of 26.7  μM. (±)-Spiro-oxanthromicin A can be isolated from soil-derived Streptomyces sp. (±)-Spiro-oxanthromicin A can mislocalize oncogenic mutant K-Ras from the plasma membrane of intact MDCK cells. (±)-Spiro-oxanthromicin A can be used for cancers research.

Z52/Z56 intermediate is a key intermediate in the synthesis of RAS inhibitors.

VVD-442 is a covalent RAS-PI3K inhibitor. VVD-442 binds covalently to cysteine 242 in the RAS binding domain of PI3K p110α and blocks RAS/PI3K interaction. VVD-442 can be used cancers like breast cancer research.

Scrambled Tadnersen is the Negative Control of Tadnersen sodium. Tadnersen sodium, an antisense oligonucleotide (ASO), selectively targets C9ORF72 transcript variants 1 and 3 that carry the expansion.

Scrambled Tadnersen sodium is the Negative Control of Tadnersen sodium. Tadnersen sodium, an antisense oligonucleotide (ASO), selectively targets C9ORF72 transcript variants 1 and 3 that carry the expansion.

OTS964 is a novel TOPK(T–lymphokine-activated killer cell–originated protein kinase) inhibitor.

DS03090629 is a potent, selective, ATP-competitive and orally available MEK1/2 inhibitor, shows high affinity for the MEK protein regardless of its phosphorylation status (npMEK (inactive) Kd=0.11 nM, and pMEK (active) Kd=0.15 nM).

ZCL279 is a small molecule modulator (SMM) that inhibits Cdc42-intersectin (ITSN) interaction. ZCL279 can activate Cdc42 (a cytoplasmic small GTPase in the Ras superfamily) at lower concentrations (<10 μM) and significantly inhibit it at higher concentrations (<10 μM).

VVD-699 is a covalent RAS-PI3K inhibitor. VVD-699 covalently binds to cysteine 242 in the RAS binding domain of PI3K p110α, thereby blocking the ability of RAS to activate PI3K activity. VVD-699 is able to inhibit the growth of RAS-mutated and HER2-overexpressing tumors. VVD-699 can be used to study cancers associated with RAS mutations (e.g., H358 lung cancer cells, A549 cells, FaDu cells).

Sosimerasib is the inhibitor for kirsten rat sarcoma viral oncogene homolog (KRAS) and exhibits antineoplastic activity.

SOF-436 is a KRAS inhibitor that inhibits SOS1-mediated KRAS nucleotide exchange (IC50 = 60 μM) and the binding of KRAS to the effector protein RAF. SOF-436 can be used in cancer research.

RMC-5127 is an orally active and brain-penetrant mutant-selective tri-complex RASG12V inhibitor. RMC-5127 non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages RASG12V(ON) to form a high-affinity tri-complex, sterically inhibiting RAS binding . RMC-5127 inhibits the RAS pathway in KRASG12V mutant cancer cells, reducing cell proliferation and inducing apoptosis. RMC-5127 is promising for research of cancers with RAS mutations, such as non-small cell lung cancer.

RMC-4998 formic is an orally active inhibitor targeting the active or GTP-bound state of the KRASG12C mutant. RMC-4998 formic can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant, with an IC50 value of 28 nM. RMC-4998 formic can inhibit ERK signaling in KRASG12C mutant cancer cells and induce apoptosis. RMC-4998 formic can be used for tumor research.

KRASG12C IN-16 (Compound SK-17) is a selective, covalent and an orally active KRASG12C inhibitor. KRASG12C IN-16 induces Apoptosis. KRASG12C IN-16 effectively prevents the activation of MAPK and PI3K/mTOR signaling pathways. KRASG12C IN-16 displays anti-tumor activity against pancreatic cancer.

KRASG12C IN-15 (Compound 21) is the orally active inhibitor for KRASG12C, and inhibits SOS1-mediated GDP/GTP exchange with an IC50 of 19 nM. KRASG12C IN-15 inhibits the phosphorylation of ERK with IC50 of 0.051 μM. KRASG12C IN-15 inhibits the cell viability of KRASG12C mutated MIA PaCa-2 with IC50 of 0.023 μM. KRASG12C IN-15 exhibits antitumor effect in MIA PaCa-2 xenograft mouse models.

INCB159020 is an orally active KRAS G12D inhibitor with a KRAS G12D SPR value of 2.2 nM. INCB159020 has antitumor activity.

Ibetazol is an inhibitor for importin β1 (KPNB1), that inhibits that binds to Cys585 of importin β1, inhibits the importin β1 mediated nuclear import with an EC50 of 6.1 µM.

AZD0022 is a selective and orally active KRASG12D inhibitor. AZD0022 inhibits KRAS pathway suppression in the GP2D xenograft model.

6-Thio-GTP (tetrasodium) is a Vav1-Rac inhibitor. 6-Thio-GTP (tetrasodium) inhibits TCR-stimulated T cell proliferation and CD28-mediated T cell survival. 6-Thio-GTP (tetrasodium) has an immunosuppressive effect in a mouse cardiac allograft transplant model and prolongs cardiac allograft survival.

Flezurafenib is an oral inhibitor of pan-RAF with potential antineoplastic activity.

Methylcarbamyl PAF C-8 is resistant to the degradation function of platelet-activating factor acetylhydrolase (PAF-AH). It has a half-life of more than 100 minutes in platelet-poor plasma and possesses the activity of inducing platelet aggregation. In NRK-49 cells overexpressing the PAF receptor, Methylcarbamyl PAF C-8 can induce the expression of c-myc and c-fos, and activate mitogen-activated protein kinase (MAPK). Additionally, Methylcarbamyl PAF C-8 can induce cell cycle arrest in the G1 phase. Methylcarbamyl PAF C-8 holds promise for research in the fields of cardiovascular diseases and anti-cancer therapy.