Toxic shock

By Targets:	HSP (2) Antibiotic (3) Bacterial (3) Biochemical Assay Reagents (1) Fungal (1) HDAC (1) IFNAR (1) IRE1 (1) Isotope-Labeled Compounds (1) NO Synthase (1) Parasite (2) Potassium Channel (1) TNF Receptor (1)
By Research Areas:	Cancer (3) Infection (4) Inflammation/Immunology (3) Neurological Disease (1)

Targets Recommended: HSP

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-139214

IXA4 2 Publications Verification	IRE1	Neurological Disease
IXA4 is a highly selective, non-toxic IRE1/XBP1s activator. IXA4 activates IRE1/XBP1s signaling without globally activating the unfolded protein response (UPR) or other stress-responsive signaling pathways (e.g., the heat shock response or oxidative stress response). IXA4 reduces secretion of APP through IRE1 activation .

HY-P4984

Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78)	Biochemical Assay Reagents	Inflammation/Immunology Cancer
Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) is a T cell proliferation activator. Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) promotes the in vitro proliferation of human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) can be used in research on inflammatory and immunity, as well as cancer .

HY-163035

EM-163	TNF Receptor IFNAR	Inflammation/Immunology
EM-163 is a summative BB-Loop analog. EM-163 can alleviate inflammation and prevent death from toxic shock by targeting the TIR domain of MyD88. EM-163 can be used in the study of SEB poisoning (SEB: Staphylococcal enterotoxin B) .

HY-115917

NOS-IN-3	NO Synthase	Inflammation/Immunology
NOS-IN-3 (Compound 9a) is a potent, selective, imidamide derived NOS inhibitor with an IC₅₀ against iNOS of 4.6 μM, without inhibiting eNOS. NOS-IN-3 has little toxicity and can be studied in the research of inducible isoform involved diseases, such as septic shock .

HY-N7118

Clindamycin hydrochloride monohydrate	Bacterial Antibiotic	Infection Cancer
Clindamycin hydrochloride monohydrate is an oral protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin hydrochloride monohydrate resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin hydrochloride monohydrate decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla) .

HY-149432

NDNA3	HSP Potassium Channel	Cancer
NDNA3 (compound 14) is a selective inhibitor of Hsp90α (IC₅₀: 0.51 μM). NDNA3 is a permanently charged analog with low membrane permeability and low toxicity to Ovcar-8 (IC₅₀: 12.66 μM) and MCF-10A (IC₅₀: 11.72 μM) cells. NDNA3 prevents disruption of hERG channel maturation without generating a heat shock response or causing degradation of Hsp90α-dependent client proteins .

HY-B1455

Clindamycin 5 Publications Verification
Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria .

HY-B1455S

Clindamycin-d3 hydrochloride	Bacterial Antibiotic Parasite	Infection
Clindamycin-d₃ (hydrochloride) is the deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2].

HY-B1455S1

Clindamycin-13C,d3	Isotope-Labeled Compounds Bacterial Antibiotic Parasite	Infection
Clindamycin- ¹³C,d₃ is the ¹³C- and deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2][3].

HY-144694

HDAC/HSP90-IN-3	HSP HDAC Fungal	Infection
HDAC/HSP90-IN-3 (compound J5) is a potent and selective fungal Hsp90 and HDAC dual inhibitor, with IC₅₀ values of 0.83 and 0.91 μM, respectively. HDAC/HSP90-IN-3 shows antifungal activity against azole resistant C. albicans. HDAC/HSP90-IN-3 can suppress important virulence factors and down-regulate drug-resistant genes ERG11 and CDR1 .

Cat. No.	Product Name	Target	Research Area

HY-P4984

Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78)	Biochemical Assay Reagents	Inflammation/Immunology Cancer
Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) is a T cell proliferation activator. Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) promotes the in vitro proliferation of human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. Toxic Shock Syndrome Toxin-1 (TSST-1) (58-78) can be used in research on inflammatory and immunity, as well as cancer .

Cat. No.	Compare	Product Name	Species	Source

HY-P71508

	TSST-1 Protein, S. aureus (His-SUMO) tst; Toxic shock syndrome toxin-1; TSST-1	Staphylococcus aureus	E. coli
	TSST-1 protein induces symptoms related to toxic shock syndrome. TSST-1 Protein, S. aureus (His-SUMO) is the recombinant Staphylococcus aureus-derived TSST-1 protein, expressed by E. coli , with N-His, N-SUMO labeled tag. The total length of TSST-1 Protein, S. aureus (His-SUMO) is 194 a.a., with molecular weight of ~37.9 kDa.


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Cat. No.	Product Name	Chemical Structure

HY-B1455S1

Clindamycin-13C,d3
Clindamycin- ¹³C,d₃ is the ¹³C- and deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2][3].

Clindamycin-13C,d3

Clindamycin- ¹³C,d₃ is the ¹³C- and deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2][3].

HY-B1455S

Clindamycin-d3 hydrochloride
Clindamycin-d₃ (hydrochloride) is the deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2].

Clindamycin-d3 hydrochloride

Clindamycin-d₃ (hydrochloride) is the deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2].

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