TCMDC-137332 is a compound that exhibits antimalarial activity against Plasmodium falciparum with an IC50 value of 7 nM.

Dimethylamiloride is a Na(+)-H+ exchange inhibitor.

JAK-IN-21 (Example 4) is a selective and potent JAK inhibitor.

Antiviral agent 17 is an anti-infection agent.

H-Val-Pro-Pro-OH (TFA) is a trifluoroacetate (TFA) salt form of the tripeptide H-Val-Pro-Pro-OH, which is derived from milk proteins. This peptide is known for its ability to inhibit Angiotensin I Converting Enzyme (ACE), a key enzyme in the renin-angiotensin system (RAS) that regulates blood pressure. The TFA salt form is commonly used in research and pharmaceutical applications to improve the solubility and stability of the peptide.

H-Val-Pro-Pro-OH is a tripeptide derived from milk proteins, specifically a proline-rich peptide, and is known for its inhibitory activity against Angiotensin I Converting Enzyme (ACE). ACE is a key enzyme in the renin-angiotensin system (RAS), which regulates blood pressure by converting angiotensin I to angiotensin II, a potent vasoconstrictor. Inhibition of ACE leads to reduced angiotensin II levels, resulting in vasodilation and lowered blood pressure.

ART-812 is a potent inhibitor of DNA polymerase Polθ (also known as Pol theta or POLQ), with an IC50 value of 7.6 nM. This indicates that ART-812 effectively inhibits the enzymatic activity of Polθ at low nanomolar concentrations. Polθ is a key enzyme involved in the microhomology-mediated end joining (MMEJ) pathway, which is an error-prone DNA repair mechanism.

17-AAG (17-N-Allylamino-17-demethoxygeldanamycin), also known by its NSC number 330507 and CP number 127374, is a well-studied inhibitor of Heat Shock Protein 90 (HSP90). HSP90 is a molecular chaperone that plays a critical role in the stabilization and activation of a wide range of client proteins, many of which are involved in oncogenic processes. By inhibiting HSP90, 17-AAG disrupts the function of these client proteins, leading to the degradation of oncogenic proteins and ultimately inhibiting cancer cell growth and survival.

FHP01 (BA103) is a potent, small molecule inhibitor of DDX3X helicase activity with IC50 of 0.3 uM in in vitro enzyme assays, exhibits very effective antiproliferative and killing activity against different breast cancer cell types (IC50=3.058 and 3.21 μM in MDA MB 468 and MDA MB 231, respectively). FHP01 does not inhibit the ATPase activity of DDX3X and the helicase activity of DDX1 (IC50>100 uM). FHP01 also inhibited WNT signaling, a key tumorigenic pathway already correlated to DDX3X functions in breast cancer model cell lines. FHP01 inhibits ER+/PR+ (IC50 = 12.43 and 10.62 μM in MCF7 and T47D cells, respectively) and HER2+ (IC50 = 13.46 μM in SKBR3) cells, but lower in control MCF10A cells (IC50 = 28.71 μM). FHP01 (45 mg/kg, i.p. injection) suppresses rowth of MDA MB 231 tumor xenografts in nude mice.

Vamotinib (PF-114) is a potent, selective and orally available inhibitor of native (IC50=0.49 nM) and mutated BCR/ABL (IC50=0.7-4 nM, ABL (T315I) IC50=0.78 nM). PF-114 potently inhibits ABL2, DDR1, DDR2, FMS, FRK, LCK, LYN and PDGFR kinases, but did not inhibit c-SRC, CSK, or c-KIT.

HTL0041178 is a potent GPR52 agonist with EC50 of 27.5 nM (human or rat GPR52).

BRD4592 is a small-molecule allosteric inhibitor that targets the tryptophan synthase (TrpAB) of Mycobacterium tuberculosis. TrpAB is a bifunctional enzyme composed of α and β subunits, which catalyzes the final steps of tryptophan biosynthesis. BRD4592 binds at the interface of the α and β subunits, disrupting the enzyme's function.

Ilunocitinib (compound 27) is a JAK inhibitor (extracted from patent WO2009114512A1).

NSC319726 is a mutant p53R175 reactivator; inhibits growth of fibroblasts expressing the p53R175 mutation (IC50 = 8 nM); shows no inhibition for p53 wild-type cells.

CBL0137 (CBL-0137) activates p53 and inhibits NF-kB with EC50s of 0.37 μM and 0.47 μM in the cell-based p53 and NF-kB reporter assays, respectively. It also inhibits histone chaperone FACT (facilitates chromatin transcription complex).

RA608 (RA-608) is a potent, selective, ATP-competitive, orally available CaMKII inhibitor, inhibits human CaMKIIδ, CaMKIIγ, CaMKIIα, and CaMKIIβ with IC50 of 22, 51, 121, and 1135 nM, respectively.RA608 displays a good selectivity profile against a broad panel of 304 human recombinant kinases.RA608 significantly reduces SR Ca leak in human atrial cardiomyocytes, reduces diastolic tension of human atrial trabeculae, does not affect action potential characteristics; attenuates heart failure in the murine HF model induced by TAC.

GS-680 (GS680) is a novel selective and ATP-competitive CaMKII inhibitor with biochemical IC50 of 2.3 and 15.9 nM against CaMKIIδ and CaMKIIα, respectively.GS-680 inhibited phospholamban phosphorylation in NRVM with an EC50 of 98.9 nM.GS-680 inhibits premature atrial contractions.GS-680 significantly reduced CaMKII autophosphorylation.GS-680 inhibits pro-arrhythmic activity in human atrium and improves contractility in failing human ventricle.

TCIP1 is the most potent transcriptional/epigenetic CIP (chemical inducers of proximity) and specifically activates BCL6 target genes. TCIP1 kills diffuse large B cell lymphoma cell lines, including chemotherapy-resistant, TP53-mutant lines and exhibits cell-specific and tissue-specific effects. TCIP1 successfully killed large B cell lymphoma cell lines, including chemotherapy-resistant TP53-mutant lines and exhibited cell-specific and tissue-specific effects. The activation of apoptosis to cell death took place in just 72 hours.BCL6 is critical to the lymphatic system, and mice engineered without the BCL6 gene die of complex inflammatory reactions. BRD4 is heavily involved in genome function and stability across many processes. Concerns regarding utilizing these important gene expressions and how they might affect off-target healthy tissues were addressed in the study.TCIP1 acts in a context-specific manner requiring the expression of BRD4 and BCL6 to both be present in order to bind them and operate at a concentration that would occupy only a tiny fraction of the total BCL6 molecules.TCIP1 induced dramatic transcriptomic changes in the spleen, notably with an upregulation of the FOXO3 gene, which mirrored activity in the targeted cancer cells. Despite the significant transcriptomic changes in the spleen, TCIP1 was well tolerated without adverse effects, with no significant differences in mouse body weight and no noticeable abnormalities such as inflammatory infiltrates or apoptotic cells. BCL6-BRD4 TCIP1 (TCIP1) is a potent BCL6-BRD4 transcriptional/epigenetic chemical inducer of proximity (TCIP) by covalently linking BCL6 binder BI-3812 to BRD4 ligand JQ1, selectively kills DLBCL cells with EC50 of 1.3 nM against KARPAS422 cell. TCIP1 rapidly and robustly killed other DLBCL lines with high levels of BCL6, but JQ1 and BI3812 separately or together shows100–1,000-fold less-effective cell killing. TCIP1 is 200–10,000-fold more potent in killing DLBCL cells than the degradation of BRD4 by dBET1 and/or degradation of BCL6 by BI3802. TCIP1 induces a stable, cooperative protein-protein interaction between bromodomain 1 (BD1) of BRD4 and the BTB domain of BCL6. TCIP1 shows affinity for intracellular ternary complex of BRD4 with Kd of 340 nM in TR-FRET assays. TCIP1 induces G1/S and G2/M block in the cell cycle, TCIP1 (10 nM) represses MYC and its targets while activating pro-apoptotic genes in KARPAS422 cells. TCIP1 kills diffuse large B cell lymphoma cell lines, including chemotherapy-resistant, TP53-mutant lines, at EC50 of 1-10 nM in 72 h and exhibits cell-specific and tissue-specific effects, capturing the combinatorial specificity inherent to transcription.

HRX-0233 (HRX0233) is a potent and selective inhibitor of MAP2K4 (MKK4), a kinase involved in the stress-activated protein kinase (SAPK) signaling pathway. MAP2K4 plays a role in regulating cellular responses to stress, apoptosis, and tumorigenesis. HRX-0233 has shown particular promise in KRAS-mutant cancers, where it exhibits synergistic effects with RAS inhibitors, making it a potential candidate for combination therapy in these difficult-to-treat cancers.

Biricodar (VX-710) is a multidrug resistance (MDR) modulator that targets two key drug efflux transporters: P-glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP-1). These transporters are often overexpressed in cancer cells and contribute to multidrug resistance (MDR) by pumping chemotherapeutic drugs out of the cells, reducing their intracellular concentration and efficacy. Biricodar inhibits the function of Pgp and MRP-1, effectively chemosensitizing multidrug-resistant cancer cells and enhancing the effectiveness of chemotherapy agents. Its ability to reverse MDR makes it a promising candidate for improving cancer treatment outcomes.

The compound you are referring to is likely a dual inhibitor of p70S6K (S6K1) and Akt, two critical kinases in the PI3K/Akt/mTOR signaling pathway. This pathway is a central regulator of cell growth, proliferation, survival, and metabolism, and its dysregulation is frequently observed in cancers, including solid tumors and non-Hodgkin's lymphoma (NHL). A dual inhibitor targeting both p70S6K and Akt would offer a powerful therapeutic strategy to block this pathway at multiple nodes, potentially overcoming resistance mechanisms and improving treatment outcomes.

IFN alpha-IFNAR-IN-1 hydrochloride is a nonpeptidic, low-molecular-weight inhibitor that specifically targets the interaction between interferon-alpha (IFN-α) and its receptor, interferon-alpha/beta receptor (IFNAR). This interaction is critical for initiating IFN-α signaling, which plays a key role in antiviral and immune responses. By blocking this interaction, IFN alpha-IFNAR-IN-1 hydrochloride inhibits IFN-α signaling and downstream responses, making it a valuable tool for studying IFN-α biology and its role in diseases such as autoimmune disorders and viral infections. It has demonstrated efficacy in inhibiting modified Vaccinia virus Ankara (MVA)-induced IFN-α responses in murine bone-marrow-derived, Flt3-L-differentiated plasmacytoid dendritic cell (pDC) cultures (BM-pDCs) with an IC50 of 2-8 µM.

Reversan (CBLC4H10) is a potent and nontoxic inhibitor of two major drug efflux transporters: multidrug resistance-associated protein 1 (MRP1) and P-glycoprotein (Pgp). These transporters are key players in multidrug resistance (MDR), a major obstacle in cancer chemotherapy, as they pump chemotherapeutic drugs out of cancer cells, reducing their intracellular concentration and efficacy. By inhibiting MRP1 and Pgp, Reversan can reverse drug resistance and enhance the effectiveness of chemotherapy agents. Its nontoxic profile makes it a promising candidate for overcoming MDR in cancer treatment.

Zelasudil is a Rho-associated coiled-coil kinase (ROCK) inhibitor with a specific binding affinity for ROCK2, a key enzyme in the Rho/ROCK signaling pathway. This pathway plays a critical role in regulating cellular processes such as cytoskeletal organization, cell motility, smooth muscle contraction, and gene expression. By selectively inhibiting ROCK2, Zelasudil modulates these processes, offering therapeutic potential for a variety of diseases characterized by fibrosis, inflammation, and vascular dysfunction, including pulmonary fibrosis, glaucoma, and cardiovascular diseases.

CMP-5 (PRMT5-IN-5) is a first-in-class, small-molecule inhibitor that specifically targets protein arginine methyltransferase 5 (PRMT5), an enzyme involved in epigenetic regulation and cellular signaling. PRMT5 catalyzes the symmetric dimethylation of arginine residues on histones and other proteins, playing a critical role in gene expression, cell proliferation, and survival. CMP-5 has shown remarkable specificity in blocking Epstein-Barr virus (EBV)-driven B-lymphocyte transformation and survival, while sparing normal B cells, making it a promising therapeutic candidate for EBV-associated cancers and other PRMT5-dependent diseases.

BI-1750 is a highly selective and stable fluorogenic substrate designed for Cathepsin C (CatC), a lysosomal cysteine protease involved in various physiological and pathological processes. Its unique properties make it a powerful tool for studying CatC activity in both research and drug development contexts.

GN13 is a potent, selective, and cell-permeable inhibitor of Gαs, with a strong binding affinity for the active, GTP-bound state of Gαs (KD = 0.19 μM). Its high selectivity and ability to penetrate cells make it a powerful tool for studying Gαs signaling in both basic research and potential therapeutic applications.

The statement suggests that CN009543V enhances tyrosine phosphorylation of the epidermal growth factor receptor (EGFR) through downstream signaling pathways.

FP802 is a novel small molecule with significant neuroprotective properties, specifically designed to target and disrupt the TwinF interface within the NMDAR/TRPM4 death signaling complex. This unique mechanism allows FP802 to selectively eliminate extrasynaptic NMDAR (eNMDAR)-mediated toxicity, which is implicated in various neurodegenerative diseases, while preserving the essential physiological functions of synaptic NMDARs. This selectivity makes FP802 a promising therapeutic candidate for conditions involving excitotoxicity and neuronal cell death.

Obtusaquinone (OBT) is a potent antineoplastic agent with significant therapeutic potential, particularly in aggressive cancers such as glioblastoma and breast cancer. Its mechanism of action involves the induction of oxidative stress and endoplasmic reticulum (ER) stress, leading to cancer cell death. OBT has demonstrated promising in vivo activity, including the ability to penetrate the blood-brain barrier (BBB) and target brain tumors, making it a particularly valuable candidate for treating central nervous system (CNS) malignancies.