regression

Sotorasib (AMG-510) is an orally active and selective covalent inhibitor of KRAS G12C. Sotorasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Sotorasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Zoldonrasib (RMC-9805) is a mutant-selective covalent KRAS G12D inhibitor with oral activity and significant antitumor activity, inducing tumor cell apoptosis in preclinical models of various KRAS-mutant cancers.

Zavondemstat (QC8222) is an orally active, selective inhibitor of the histone lysine demethylase 4 (KDM4) family, with an IC₅₀ of ≤ 0.08 μM against human KDM4A–D and a K₊₀ of 0.52 μM against human KDM4C. Zavondemstat activates tumor suppressor genes, induces apoptosis, causes S-phase cell cycle arrest, and inhibits cancer cell proliferation. In in vivo studies, Zavondemstat inhibits tumor growth and induces tumor regression. Zavondemstat can be used in cancer research.

MSA-2 is an orally available non-nucleotide STING agonist. The non-covalent dimer of MSA-2 binds to STING with nanomolar affinity. It shows anti-tumor activity in syngeneic mouse tumor models, synergizes with anti-PD-1, stimulates tumor secretion of interferon-β, induces tumor regression, and has long-lasting anti-tumor immunity. [3]

GGTI-2418 is a highly potent, competitive, and selective inhibitor of geranylgeranyltransferase I (GGTase I), exhibiting inhibitory activities with IC50 values of 9.5 nM for GGTase I and 53 μM for FTase, respectively. Additionally, it enhances p27(Kip1) expression and induces significant regression of breast tumors.

YPC-22026 has potential anticancer activity, inducing tumor regression in a mouse xenograft model while inhibiting ZNF143-regulated genes.

(S)-Enitociclib (VIP152) is a selective CDK9 inhibitor that induces complete regression of MYC+ lymphomas by inhibiting RNA polymerase II-mediated transcription of anti-apoptotic and pro-survival proteins.

GDC-0425 (RG-7602) is a potent and highly selective inhibitor of Checkpoint kinase 1 (Chk1). This product blocks DNA damage-induced cell cycle arrest by inhibiting Chk1 activity, forcing damaged cells into mitosis and ultimately leading to apoptosis. Research indicates that the activity of GDC-0425 is modulated by the Ras-MEK signaling pathway, and it significantly enhances tumor regression when combined with DNA-damaging agents like Gemcitabine.

Tetracycline is an orally active broad-spectrum antibiotic that exhibits inhibitory activity against various Gram-positive and Gram-negative bacteria, as well as Chlamydia, Mycoplasma, and Rickettsia. It is commonly used in anti-infection research and can also be used to induce tumor regression based on BCR-ABL gene silencing.

Increased levels of erucic acid (22:1n9) have been found in the red blood cell membranes of autistic subjects with developmental regression (PMID: 16581239 ). Erucic acid (13(Z)-Docosenoic Acid) is broken down long-chain acyl-coenzyme A (CoA) dehydrogenase, which is produced in the liver. This enzyme breaks this long chain fatty acid into shorter-chain fatty acids. human infants have relatively low amounts of this enzyme and because of this, babies should not be given foods high in erucic acid. Erucic acid is found to be associated with isovaleric acidemia, which is an inborn error of metabolism.

AMG410 is a non-covalent, dual-modality KRAS inhibitor effective against both GDP (OFF) and GTP (ON) binding, with Kd (GDP) of 1 nM and Kd (GTP) of 22 nM, capable of blocking KRAS independently of the cell cycle. AMG410 does not affect HRAS and NRAS2, and exhibits high potency against KRAS G12D, G12V, G12C, G13D, and other mutants, with an IC₅₀ of 1–4 nM. It induces tumour regression and reduces phosphorylated ERK levels in KRAS-mutant cancer models.

BMS-986463 is a WEE1 kinase molecule gel degrader and a CRBN E3 ligase regulator (CELMoD). BMS-986463 significantly inhibits tumor regression and reduces the level of phosphorylated CDK2. BMS-986463 is utilized in oncology research involving cell-cycle checkpoint regulation, protein degradation pathways, and malignant solid tumor models including non-small cell lung cancer (NSCLC).

TYRA-200 is an orally active FGFR1/2/3 inhibitor that induces dose-dependent tumor regression in wild-type and mutant FGFR2 models, making it a candidate for advanced or metastatic intrahepatic cholangiocarcinoma.

MOMA-341 is a selective, ATP-competitive WRN allosteric inhibitor that binds to the cysteine 727 site of WRN. It induces DNA damage, cell death, and tumor regression in dMMR/MSI-H mouse models and can be used to study advanced and metastatic solid tumors.

LY2457546 is a highly potent, orally bioavailable multi-target anti-angiogenic tyrosine kinase inhibitor. It shows strong inhibitory activity against multiple targets including VEGFR2, PDGFRβ, FLT-3, Tie-2, and Eph family receptors, and is applied in cancer research such as leukemia.

ecMetAP-IN-1 can be used as a QSAR model to study methionine aminopeptidase inhibitor as an anticancer agent using multiple linear regression.

ADU-S100 ammonium salt is an activator of stimulator of interferon genes (STING). ADU-S100 ammonium salt leads to potent and systemic tumor regression and immunity.

SIAIS178 is a selective PROTAC degrader targeting BCR-ABL with an IC50 of 24 nM. It degrades BCR-ABL protein by recruiting the VHL E3 ubiquitin ligase, inhibiting leukaemia cell growth in vitro and causing regression of K562 xenograft tumours.

Estrogen receptor modulator 1 causes regression of Tamoxifen-resistant, hormone-independent xenograft tumors. Estrogen receptor modulator 1 is an orally active and selective estrogen receptor modulator (SERM) (pIC50: 0.46).

Sograzepide (Netazepide) is an orally active, selective and highly potent gastrin/CCK-B antagonist that inhibits gastrin/CCK-A activity and pappalysin 2 expression in type 1 gastric neuroendocrine tumors, and can induce regression of type 1 gastric neuroendocrine tumors.

HRX-0233 is a small-molecule MAP2K4 inhibitor that induces strong tumor regression without apparent toxicity in KRASG12C-mutant non-small cell lung cancer models, prevents receptor tyrosine kinase feedback activation during sotorasib monotherapy. HRX-0233 achieves sustained MAPK pathway suppression, supporting its application in lung, colon, and AR-negative prostate cancer research.

DS06652923 is an orally active inhibitor targeting EGFR triple mutations. It exhibits growth-inhibitory effects on Ba/F3EGFRdel19/T90M/C795S cells, with a GI50 value of 9.4 nM. Additionally, DS06652923 induces tumor regression in the Ba/F3 syngeneic transplantation model.

DNMT1/HDAC-IN-1 (compound (R)-23a), a potent dual inhibitor targeting both DNMT1 and HDAC, exhibits impressive inhibitory effects specifically on HDAC1 (HDAC1:IC50=0.05 μM), a major HDAC isoform that interacts with DNMT1 across multiple protein complexes involved in the transcriptional silencing of TSGs. This compound has been shown to remodel the tumor immune microenvironment and induce tumor regression, effectively reversing cancer-specific epigenetic abnormalities.

MD-265 is a PROTAC degrader that targets and degrades MDM2, leading to the activation of p53 in cancer cells with wild-type p53. MD-265 achieves complete tumor regression and enhances long-term survival in leukemic mice.