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.

AMG410 is a non-covalent and selective pan-KRAS inhibitor with IC50 values of 1-4 nM for KRAS G12D, KRAS G12V, and KRAS G13D. AMG410 shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 is a dual GTP(on)- and GDP(off)-state inhibitor (Kd(GDP-state) of 1 nM; Kd(GTP-state) of 22 nM). AMG410 blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 can be used for the study of colorectal, pancreatic, and lung cancers.

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.

IODVA1 is a small molecule with cellular inhibitory activity against several transformed cell lines including Ras-driven cells, targets Rac activation and signaling instead of Ras; IODVA1 inhibits ST8814 cell proliferation with GI50 of 1 uM, similar results were observed with MCF7, MDA-MB-231, and T47D cells with estimated GI50s <1 uM. IODVA1 significantly decreases number of colonies of the breast cancer cells in soft agar at 1 and 3 uM. IODVA1 probably does not bind Ras and that its mechanism of action is likely Ras-independent, inhibits lamellipodia and circular dorsal ruffle (CDR) formation in MDA-MB-231 cells and decreases Rac activation. IODVA1 inhibits Rac activation and downstream signaling leading to inhibition of lamellipodia and CDR formation; IODVA1 inhibits cell-substratum and cell-cell interactions, does not target kinases, and reduces tumor burden of solid tumors in vivo.

BC-DXI-32982 is a potent inhibitor of the interaction between DX2 and KRAS4B with a half-maximal inhibitory concentration (IC50) of 0.18 μM, showing little effect on the PRKACA-PRKAR2A interaction.

DW0254 (DW-0254,DW 0254) is a small molecules capable of inhibiting RAS-related C3 botulinum toxin substrate (RAC) small GTPase activation in ALL cell lines, directly binds to the hydrophobic pocket of PDE6D (Kd=436 nM, ITC), a RAS chaperone protein.DW0254 demonstrated dose-dependent RAC inhibition, arrest of proliferation and induced apoptosis in human leukemic cell lines (RS4;11 IC50=1.5-1.8 uM), also showed promising anti-leukemic activity in RAS-mutated cells (CCRF-CEM NRAS G12D, IC50=3.3-4.2 uM).DW0254 disrupted the interaction between PDE6D and RAS, disturbing RAS subcellular localization.DW0254 demonstrated anti-leukemic activity, decreased tumor progression in a murine xenograft model.

KAL-21404358 (KAL21404358) is a small-molecule, allosteric inhibitor of K-Ras(G12D), binds to K-Ras(G12D) P110 site with KD of 88 uM in MST assay; KAL-21404358 disrupts the K-RasG12D-B-Raf interaction using a NanoBiT split luciferase assay, and to impair the Raf-MEK-ERK and the PI3K-AKT signaling pathways. KAL-21404358 exhibited specificity for K-RasG12D over K-RasWT, H-RasWT, Rap1a, R-Ras and R-Ras2.

Ras binder 2C07 is a switch-II binding ligand which binds Ras GDP and GTP states.

RMC-4998 (RMC4998) is a tricomplex inhibitor that targets the active state or GTP-bound state of KRAS G12C, selectively inhibits the proliferation of KRASG12C mutant cells with mean IC50 of 0.28 nM.

Antineoplaston A10 is a naturally occurring substance in the human body that that can be potentially used for the treatment of glioma, lymphoma, astrocytoma and breast cancer. The main ingredient active of antineoplaston A10 (Phenylacetylglutamine, PG) inhibits RAS and promotes apoptosis.

LY3537982 (KRAS G12C inhibitor 19) is a highly selective and potent inhibitor of the  KRAS-G12C protein. LY3537982 selectively inhibits the growth of KRAS G12C mutant cells H23 G12C, H358 G12C, and H2122 G12C with IC50s of 1.04 nM, 1.16 nM, and 11.38 nM, respectively.

SIJ1795 is a potent mutated RAS (mtRAS)-signaling pathway blocker/inhibitor with IC50 of 82 and 75 nM for Ba/F3-NRAS-G12D and Ba/F3-NRAS-G12V, respectively.

SIJ1772 is a potent mutated RAS (mtRAS)-signaling pathway blocker/inhibitor with IC50 of 77 and 96 nM for Ba/F3-NRAS-G12D and Ba/F3-NRAS-G12V, respectively.

SCH-53239 (SCH53239) is a small molecule inhibitor of Ras nucleotide exchange with IC50 of 0.5 uM, bind competitively with GDP in the nucleotide binding site of the Ras protein.

RSC-1255 (KRAS inhibitor 249C, V-ATPase inhibitor) is a Ras-mutant selective cytotoxic agent with nanomolar potency against a spectrum of Ras-mutant cancer cells (A549 (KRASG12S), IC50=73 nM), binds to V-ATPase (Kd=23 nM) and inhibits its activity.

G12Si-5 is a specific small molecule that covalently target K-Ras(G12S) mutation, suppresses K-Ras(G12S) signaling, preferentially inhibits the growth of the K-Ras(G12S)-transduced cells with IC50 of 2.4 uM.

Fulzerasib is a potent selective inhibitor of KRAS gene mutation.

ERAS-5024 (ERAS5024) is a potent and selective KRAS G12D inhibitor with IC50 of 0.86 nM in RAS-RAF binding assays, inhibits ERK1/2 phosphorylation (pERK) formation with IC50 of 2.1 nM in AsPC-1 cell-based assays.

CSC01 is a small molecule inhibitor of oncogenic KRAS mutant G13D (KRAS-G13D).

BBO-8956 is a highly potent, covalent inhibitor of GTP-KRAS G12C, BBO-8956 is effective against both GDP and GTP-bound KRAS G12C.