Yimitasvir (Emitasvir) is an orally active hepatitis C virus (HCV) nonstructural protein 5A (NS5A) inhibitor. Yimitasvir can be used for research of chronic HCV infection[1].

YJ182 is a NDM-1 inhibitor (IC50: 0.23 μM). YJ182 also inhibits IMP-1, VIM-2, GIM-1, and MMP-2, with IC50s of 0.25, 0.61, 0.49, and 6.92 μM respectively. YJ182 can be used for bacterial infection research[1].

YJ196 (Compound 59) is a New Delhi Metallo-β-lactamase-1 (NDM-1) inhibitor[1].

YK-029A is an orally active inhibitor of mutant EGFR，targeting to both the T790M mutations (EGFRT790M) and exon 20 insertion of EGFR (EGFRex20ins). YK-029A exhibits significant antitumor activity，and results tumor regression in EGFRex20ins-driven PDX models[1].

YK-029A is an orally active inhibitor of mutant EGFR，targeting to both the T790M mutations (EGFRT790M) and exon 20 insertion of EGFR (EGFRex20ins). YK-029A exhibits significant antitumor activity，and results tumor regression in EGFRex20ins-driven PDX models[1].

YK-029A is an orally active inhibitor of mutant EGFR，targeting to both the T790M mutations (EGFRT790M) and exon 20 insertion of EGFR (EGFRex20ins). YK-029A exhibits significant antitumor activity，and results tumor regression in EGFRex20ins-driven PDX models[1].

YK-029A is an orally active inhibitor of mutant EGFR，targeting to both the T790M mutations (EGFRT790M) and exon 20 insertion of EGFR (EGFRex20ins). YK-029A exhibits significant antitumor activity，and results tumor regression in EGFRex20ins-driven PDX models[1].

YKL-04-085 is potent inhibitors of viral translation, with an IC90 of 0.555 μM for DENV2. YKL-04-085 is devoid of any kinase activity[1].

YKL-1-116 is a selective and covalent inhibitor of Cdk7. YKL-1-116 does not target Cdk9, Cdk12, or Cdk13. YKL-1-116 is more potent than THZ1 (HY-80013) toward both Cdk7WT and Cdk7as, although Cdk7as is relatively resistant to this compound as well[1].

YL-365 is a angonist of GPR34. YL-365 is used for pain and cancer research[1].

YL5084, a covalent JNK inhibitor, exhibits selectivity for JNK2 and JNK3 over JNK1 with IC50s of 70 nM, 84 nM and 2173 nM, respectively. YL5084 exhibits JNK2-independent antiproliferative effects and induces apoptosis in a JNK2-independent manner[1].

YL93 is a dual inhibitors of MDM2/4 with Ki values of 0.64 μM and 1.1 nM for MDM4 and MDM2, respectively. YL93 induces cell-cycle arrest and apoptosis. YL93 shows p53-dependent cell growth inhibition[1].

YLADGDLHSDGPGR is a polypeptide that can be found by peptide screening. Peptide screening is a research tool that pools active peptides primarily by immunoassay. Peptide screening can be used for protein interaction, functional analysis, epitope screening, especially in the field of agent research and development[1].

YLLEMLWRL is an HLA-A2-restricted T cell epitope sequence corresponding to codon 125-133. Among them, YLLEMLWRL sequence is the main mutation site of HLA-A2-restricted CTL epitope sequence[1].

YLT-11 is a potent, selective and orally active PLK4 inhibitor with Kd values of >10000, 653, >10000, 5.2 nM for PLK1, PLK2, PLK3, PLK4, respectively. YLT-11 shows antiproliferative activity. YLT-11 induces Apoptosis and cell cycle arrest at G2/M phase. YLT-11 show anticancer activity[1].

YM Agar is a low pH growth medium for the cultivation of yeasts, molds and other acid-resistant microorganisms[1].

YM-08 (Compounds 7a) is a brain-penetrant inhibitors of SIRT2,with the IC50 of 19.9 μM. YM-08 also is inhibitor of Hsp70[1].

YM-1 is a stable and soluble MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins[1][2].

YM-1 is a stable and soluble MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins[1][2].

YM-1 is a stable and soluble MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins[1][2].

YM-1 is a stable and soluble MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins[1][2].

YM-1 is a stable and soluble MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins[1][2].

YM11 Agar is a special agar for isolation and culture of mold and yeast. The composition of 1 litre medium is 47.5 g YM11 Agar [1].

YM543 free base is a potent and orally active sodium-glucose cotransporter (SGLT) 2 inhibitor. YM543 free base reduces blood glucose levels. YM543 free base can be used in research of diabetes[1][2].

YN14 is a KRASG12C proteolysis targeting chimera (PROTAC). YN14 is highly potent and selective KRASG12C degrader and induces a stable KRASG12C: YN14: VHL ternary complex with low binding free energy (ΔG). YN14 has antiproliferative effects and significantly inhibits KRASG12C-mutant cancer cell growth. YN14 leads to tumor regression with tumor growth inhibition (TGI%) rates more than […]

YNPCVMYL (Thioester: Cys4-Leu8) TFA is a polypeptide chain of the YNPCVMYL sequence. The link between the fourth and eighth amino acids in the sequence has the properties of a thioester, which is formed between cysteine (Cys4) and leucine (Leu8).

YNPCVMYL (Thioester: Cys4-Leu8) is a polypeptide chain of the YNPCVMYL sequence. The link between the fourth and eighth amino acids in the sequence has the properties of a thioester, which is formed between cysteine (Cys4) and leucine (Leu8).

YO-PRO-1 (Oxazole yellow) is a carbocyanine monomer and DNA green fluorescent dye that is not permeable to normal animal cell membranes but is permeable to the cell membranes of apoptotic and necrotic cells. YO-PRO-1 is commonly used for the detection of apoptosis and necrosis. YO-PRO-1 has a high affinity for DNA and is essentially non-fluorescent […]

Yohimbine-d3 is the deuterium labeled Yohimbine (HY-12715)[1].

Yohimbine-d3 is the deuterium labeled Yohimbine (HY-12715)[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer’s disease[1].

YOYO-3 is a cell-impermeant dye with far-red fluorescence used as nulear counterstain and dead cell indicator. It generates bright fluorescence upon binding to DNA.

Yp537 TFA is an estrogen receptor (ER) inhibitor that blocks dimerization of the human estrogen receptor[1].

Yp537 TFA is an estrogen receptor (ER) inhibitor that blocks dimerization of the human estrogen receptor[1].

Yp537 TFA is an estrogen receptor (ER) inhibitor that blocks dimerization of the human estrogen receptor[1].

YPX-C-05 is a hydroxamic acid-based HDAC inhibitor. YPX-C-05 exerts significant vasodilatory effects. YPX-C-05 exhibits inhibitory effects on HDACs and increases histone H4 acetylation in endothelial cells. YPX-C-05 can be used for hypertension research[1].

YQA14 is a high affinity dopamine D3 receptor antagonist. YQA14 is anti-opioid addiction agent. YQA14 inhibits Morphine/Cocaine-induced conditioned place preference (CPP) in animals[1][2].

YS 035 hydrochloride is a Ca2+ antagonist on cellular uptake and mitochondrial efflux of calcium ions. YS 035 hydrochloride inhibits Ca2+ uptake by muscle cells and inhibits Na+/Ca2+ exchange (Ki=28 µM). YS 035 hydrochloride is a useful tool for research on the mitochondrial Ca2+ transport[1].

YS-363 is a potent, selective, and orally active EGFR inhibitor, with IC50s of 0.96 nM and 0.67 nM for wild-type and L858R mutant forms of EGFR, respectively. YS-363 can induce G0/G1 cell cycle arrest and apoptosis[1].