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Z-VAD-FMK (Caspase Inhibitor VI) is a broad-spectrum inhibitor of caspases.Z-VAD-FMK binds to activated caspases and inhibits apoptosis.Z-VAD-FMK does not inhibit UCHL1 activity, even at concentrations up to 440 μM.

Phytochelatin 2, a short plant peptide, serves as an essential metal-binding compound. Phytochelatins are a diverse group of plant compounds that play a crucial role in chelating metals, safeguarding against metal toxicity, and maintaining metal homeostasis.

Phytochelatin 6 TFA, a metal-binding compound synthesized by plants, can potentially decrease the bioavailability of dietary toxic metals like cadmium [1].

Phytochelatin 6, a metal-binding compound synthesized by plants, can potentially decrease the bioavailability of dietary toxic metals, including cadmium [1].

Phytochelatin 5 TFA, a metal-binding compound produced by plants, may reduce the bioavailability of dietary toxic metals, such as cadmium [1].

Phytochelatin 5, a metal-binding compound synthesized by plants, can potentially diminish the bioavailability of dietary toxic metals, including cadmium [1].

Phytochelatin 4 (PC 4) TFA is a cysteine-rich, plant-derived peptide characterized by repetitive γ-glutamyl-cysteine motifs [1].

Phytochelatin 4 (PC 4) a glutathione derived peptide and heavy metal detoxifier chelator consisting of 4 units of glu - cys and generated by PC synthase, is tolerant to Cd (cadmium) and is sequestered in vesicles after complexation with heavy metals.

Phytochelatin 3 (PC 3) TFA is a small peptide renowned for its metal-chelating properties, particularly in binding heavy metals [1].

Phytochelatin 3 (PC3) is a glutathione-derived peptide and heavy metal detoxifier chelator consisting of 3 units of glu-cys.

Phytochelatin 2 (PC2) TFA, a heavy metal-binding peptide, facilitates metal chelation, mitigates metal toxicity, and promotes metal homeostasis within internal environments [1].

S-trityl-L-Cysteine is a non-natural amino acid and an inhibitor of Eg5, also known as KSP and Kif11, a mitotic kinesin necessary for mitotic spindle formation. S-trityl-L-Cysteine inhibits the ATPase activity of Eg5 in basal and microtubule-stimulated states (IC50s = 1,000 and 140 nM, respectively). It is selective for Eg5 over nine other human kinesins in an enzyme-coupled assay. It reversibly inhibits Eg5-driven microtubule sliding velocity with an IC50 value of 500 nM using X. laevis recombinant Eg5. It induces cell cycle arrest in HeLa cells (IC50 = 700 nM), reversibly halting the cell cycle in the mitotic phase by inhibiting the separation of duplicated chromosomes and preventing bipolar spindle formation. S-trityl-L-Cysteine inhibits the growth of cancer cells in vitro when tested against the National Cancer Institute (NCI) 60 human cancer cell line panel (average GI50 = 1.3 μM) and in mouse xenograft models.

L-Selenocystine (L-Selenocystine) can be used as a building block in biologically active selenol compounds.

Cyclo(Gly-His) is a cyclic dipeptide encompassed within liposomes, exhibiting antimicrobial and anticancer properties with cytotoxic effects on HeLa and MCF-7 cells, demonstrating IC50 values of 1.699 mM and 0.358 mM, respectively. This compound is relevant for drug delivery system research [1].

Caerin 1.1 TFA, a host defense peptide derived from the Australian tree frog Litoria's glandular secretions, exhibits anti-proliferative effects on HeLa cells and induces apoptosis. Additionally, it has the potential to augment adaptive T cell immune responses [1].

BRC4wt, an acetylated peptide originating from the BRC4 repeat within human BRCA2 (1521-1536), acts as an inhibitor of the BRCA2 and RAD51 protein-protein interaction. When linked to the cationic cell-penetrating peptide (Arg)9, it effectively shortens DNA replication tract lengths and diminishes the frequency of homologous repair of camptothecin-induced DNA damage in vitro. Additionally, BRC4wt enhances the efficacy of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib in inducing cell death in HeLa human cervical cancer and U2OS human osteosarcoma cells, albeit it does not affect non-cancerous hTERT RPE-1, MRC-5, or MCF-10A cells.

Peptide comprising residues 33 - 57 of the JNK binding (δ) domain of human c-Jun. Disrupts JNK/c-Jun interaction leading to inhibition of serum-induced c-Jun phosphorylation, up-regulation of p21cip/waf and modulation of inflammatory gene expression. Spec

IP3RCYT is an inhibitory peptide of IP3R that can prevent cytochrome C from binding with IP3R, with an IC50 of approximately 100 nM. It regulates intracellular calcium signaling. Additionally, IP3RCYT inhibits apoptosis in HeLa and Jurkat cells treated with staurosporine or membrane-bound Fas ligand (FasL).