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conditionally

" in MedChemExpress (MCE) Product Catalog:

21

Inhibitors & Agonists

4

Inhibitory Antibodies

8

Natural
Products

8

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-Y0337
    L-Cysteine
    3 Publications Verification

    Cysteine

    		 Endogenous Metabolite Metabolic Disease
    L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans .
    L-Cysteine
  • HY-W016715
    L-Cysteine hydrochloride hydrate
    3 Publications Verification

    		 Endogenous Metabolite Metabolic Disease
    L-Cysteine hydrochloride hydrate is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine hydrochloride hydrate suppresses ghrelin and reduces appetite in rodents and humans .
    L-Cysteine hydrochloride hydrate
  • HY-P99572
    Tecaginlimab

    BNT-312; DuoBody-CD40x-4-1BB; GEN1042

    		 TNF Receptor Inflammation/Immunology Cancer
    Tecaginlimab (BNT-312) is a Fc-inert bispecific antibody for dual targeting and conditional stimulation of CD40 and 4-1BB. Tecaginlimab can enhance priming and reactivation of tumor-specific immunity .
    Tecaginlimab
  • HY-Y0337S5
    L-Cysteine-d3

    		Isotope-Labeled Compounds Endogenous Metabolite Metabolic Disease
    L-Cysteine-d3 is the deuterium labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-d3
  • HY-Y0337S6
    L-Cysteine-d2

    		Isotope-Labeled Compounds Endogenous Metabolite Metabolic Disease
    L-Cysteine-d2 is the deuterium labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-d2
  • HY-Y0337S1
    L-Cysteine-15N

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine- 15N is the 15N-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-15N
  • HY-Y0337S4
    L-Cysteine-13C3

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine- 13C3 is the 13C-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-13C3
  • HY-P9988
    Mecbotamab

    BA301

    		 ADC Antibody TAM Receptor Cancer
    Mecbotamab is a humanized IgG1-κ antibody targeting to AXL receptor tyrosine kinase (AXL). Mecbotamab can serves as a conditionally active biologic (CAB), which can be conjugated with MMAE (HY-15162) via a cleavable linker, to form ADC Mecbotamab vedotin (BA3011) .
    Mecbotamab
  • HY-Y0337R
    L-Cysteine (Standard)

    		Endogenous Metabolite Metabolic Disease Cancer
    L-Cysteine (Standard) is the analytical standard of L-Cysteine. This product is intended for research and analytical applications. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans .
    L-Cysteine (Standard)
  • HY-P990067
    Evunzekibart

    ATOR-1017

    		 TNF Receptor Cancer
    Evunzekibart (ATOR-1017) is an Fc-γ receptor conditional 4-1BB agonist and IgG4-type antibody. Evunzekibart can be used as monotherapy or in combination with anti-PD1 to exert anticancer activity.
    Evunzekibart
  • HY-W016715R
    L-Cysteine hydrochloride hydrate (Standard)

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine (hydrochloride hydrate) (Standard) is the analytical standard of L-Cysteine (hydrochloride hydrate). This product is intended for research and analytical applications. L-Cysteine hydrochloride hydrate is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine hydrochloride hydrate suppresses ghrelin and reduces appetite in rodents and humans .
    L-Cysteine hydrochloride hydrate (Standard)
  • HY-Y0337S2
    L-Cysteine-3-13C

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine-3- 13C is the 13C-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-3-13C
  • HY-Y0337S3
    L-Cysteine-1-13C

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine-1- 13C is the 13C-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-1-13C
  • HY-Y0337S
    L-Cysteine-13C3,15N

    		Endogenous Metabolite Metabolic Disease
    L-Cysteine- 13C3, 15N is the 13C- and 15N-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-13C3,15N
  • HY-Y0337S7
    L-Cysteine-d3,15N

    		Isotope-Labeled Compounds Endogenous Metabolite Metabolic Disease
    L-Cysteine-d3, 15N is the deuterium and 15N-labeled L-Cysteine. L-Cysteine is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine suppresses ghrelin and reduces appetite in rodents and humans[1].
    L-Cysteine-d3,15N
  • HY-P99419
    Acasunlimab

    GEN1046

    		 PD-1/PD-L1 Cancer
    Acasunlimab (GEN1046) is a bispecific antibody (bsAb) targeting PD-L1 and 4-1BB. Acasunlimab enhances T-cell and NK-cell function through conditional 4-1BB stimulation while constitutively blocking the PD-1/PD-L1 inhibitory axis. Acasunlimab can be used in research of cancer .
    Acasunlimab
  • HY-112210
    Shield-1
    3 Publications Verification

    Shld1

    		 FKBP Others
    Shield-1 (Shld1) is a specific, cell-permeant and high-affinity ligand of FK506-binding protein-12 (FKBP), and reverses the instability by binding to mutated FKBP (mtFKBP), allowing conditional expression of mtFKBP-fused proteins. Shield-1 can stabilize proteins tagged with a mutated FKBP12-derived destabilization domain (DD) .
    Shield-1
  • HY-Y0337A
    L-Cysteine hydrochloride
    3 Publications Verification

    		 Endogenous Metabolite Metabolic Disease
    L-Cysteine hydrochloride is an orally active conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine hydrochloride suppresses ghrelin and reduces appetite in rodents. L-Cysteine hydrochloride inhibits Aspergillus flavus growth and AFB synthesis by disrupting cell structure and antioxidant system balance. L-Cysteine hydrochloride enhances relaxant responses of rat aortic rings to NO and reduces responses to endothelium-derived relaxing factor (EDRF) .
    L-Cysteine hydrochloride
  • HY-Y0337AR
    L-Cysteine hydrochloride (Standard)

    		Endogenous Metabolite Metabolic Disease Cancer
    L-Cysteine (hydrochloride) (Standard) is the analytical standard of L-Cysteine (hydrochloride). This product is intended for research and analytical applications. L-Cysteine hydrochloride is an orally active conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), glutathione and taurine. L-Cysteine hydrochloride suppresses ghrelin and reduces appetite in rodents. L-Cysteine hydrochloride inhibits Aspergillus flavus growth and AFB synthesis by disrupting cell structure and antioxidant system balance. L-Cysteine hydrochloride enhances relaxant responses of rat aortic rings to NO and reduces responses to endothelium-derived relaxing factor (EDRF) [4].
    L-Cysteine hydrochloride (Standard)
  • HY-157288
    (R)-Phe-A110/B319

    		Others Metabolic Disease
    (R)-Phe-A110/B319, a hapten, is a selective binder to tumor-associated antigens. (R)-Phe-A110/B319 has a 20-fold higher affinity towards the H1047R mutant of p110α in the p110α/p85α PI3K complex. (R)-Phe-A110/B319 can be used for the research of conditional chimeric antigen receptor T (CAR-T) cell activation and tumor targeting .
    (R)-Phe-A110/B319
  • HY-117051
    STA-2842

    		Others Cancer
    STA-2842 is a small molecule agent that inhibits heat shock protein 90 (HSP90) to treat autosomal dominant polycystic kidney disease (ADPKD). The disease is caused by inherited mutations in the PKD1 or PKD2 genes that aberrantly activate multiple signaling proteins and pathways that regulate cell proliferation. Through network construction, we found that many HSP90 client proteins associated with ADPKD are regulated by HSP90. STA-2842 induced degradation of these clients in Pkd1?/? primary kidney cells and in vivo. In experiments using conditional Cre-mediated in vivo knockout of Pkd1 in mice, we found that weekly administration of STA-2842 for 10 weeks significantly reduced initial renal cyst formation and kidney growth in mice and slowed disease progression in mice with pre-existing cysts. These improved disease phenotypes were accompanied by improvements in renal function markers and reductions in the expression and activity of HSP90 clients and their effectors, with the extent of this inhibition correlating with the extent of cyst expansion in individual animals. Pharmacokinetic analysis showed that HSP90 was overexpressed in cystic kidney tissue and HSP90 inhibitors were selectively retained in cystic tissue, which is similar to the situation in solid tumors. These results provide a preliminary basis for evaluating HSP90 inhibitors as therapeutic agents for ADPKD.
    STA-2842

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