SP187 hydrochloride
Based on 3 publication(s) in Google Scholar
SP187 hydrochloride (MON-DNJ hydrochloride; UV4 hydrochloride) is an orally active, host-targeting iminosaccharide against filovirus infection. SP187 hydrochloride inhibits endoplasmic reticulum glucosidase. SP187 hydrochloride exhibits antiviral and Dengue Virus activity in vivo. SP187 hydrochloride can be used in antiviral and dengue research.
For research use only. We do not sell to patients.
- CAS No.: 1333144-07-2
- Formula: C16H34ClNO5
- Molecular Weight:355.90
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Publications Citing Use of MedChemExpress (MCE) SP187 hydrochloride
More
Biological Activity
Description
Chemical Information
-
CAS No. 1333144-07-2
-
Molecular Weight 355.90
-
Formula C16H34ClNO5
-
SMILES
OC[C@H]1N(C[C@H](O)[C@@H](O)[C@@H]1O)CCCCCCCCCOC.Cl
-
Synonyms
MON-DNJ hydrochloride; UV4 hydrochloride
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (3)
-
Journal Impact Factor
-
Most Recent
-
J Exp Clin Cancer Res
Mutant p53-ENTPD5 control of the calnexin/calreticulin cycle: a druggable target for inhibiting integrin-α5-driven metastasis. [Abstract]2023 Aug 10;42(1):203. PMID: 37563605 -
ACS Cent Sci
Epi-Cyclophellitol Cyclosulfate, a Mechanism-Based Endoplasmic Reticulum α-Glucosidase II Inhibitor, Blocks Replication of SARS-CoV-2 and Other Coronaviruses. [Abstract]2024 Jul 25;10(8):1594-1608. PMID: 39220688 -
Glycobiology
2021 May 3;31(4):378-384. PMID: 32985653
Protocols
-
Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
SP187 hydrochloride Related Classifications
HY-108023 Related Classifications
Powered by Bioz