75580-37-9 Usage
Uses
Used in Pharmaceutical Industry:
BBM-928 A is used as an antitumor and antibiotic agent for its potent activity against a variety of experimental tumors. It acts as a bifunctional DNA intercalator, strongly binding to DNA and forming crosslinks between DNA molecules, which contributes to its antitumor properties.
BBM-928 A is also used as an inhibitor of HIV-1 and HIV-2 reverse transcriptase, with IC50s of 7 and 68 nM, respectively. This makes it a valuable compound in the development of treatments for HIV.
Used in Cosmetic Industry:
BBM-928 A is used as a key ingredient in cosmetic formulations for its beneficial properties for skin health. It may be utilized for its potential anti-aging, moisturizing, or skin-soothing effects, depending on the specific formulation and intended use.
Biological Activity
luzopeptin a is a cyclic depsipeptide antibiotic.a depsipeptide is a peptide in which one or more of its amide groups are replaced by the corresponding ester, or more generally, is a molecule that has both peptide and ester linkages in proximity in the same amino acid-containing small molecule or chain.
in vitro
previous study found that luzopeptin a treatment could produce additional dna bands which were the products of type ii biintercalation. the types of restriction fragments involved were identified. maximal type ii biintercalation occurred at a luzopeptin a/dna range of 0.14 to 0.18, at which more than 50% of the total dna molecules were involved. type ii products were gradually converted to type i products upon prolonged incubation at 37 degrees, maybe due to the tendency for intermolecular bonds to disrupt. echinomycin treatment failed to produce type ii products, probably because of a dna-binding affinity weaker than that of luzopeptin a [1].
in vivo
animal study showed that when administered as a suspension in 0.9% nacl solution, luzopeptin a demonstrated good activity against i.p. b16 melanoma and i.p. p388 leukemia and weak activity versus i.v. p388, i.p. l1210 leukemia, lewis lung, and madison 109 lung carcinomas. in terms of tumor cell kill, luzopeptin a induced net reductions in the body burdens of l1210 and p388 leukemias following single-drug injections but failed to yield net reductions following multiple-injection therapies [2].
references
[1] huang, c. h.,mirabelli, c.k.,mong, s., et al. intermolecular cross-linking of dna through bifunctional intercalation of an antitumor antibiotic, luzopeptin a (bbm-928a). cancer research 43, 2718-2724 (1983).[2] rose wc, schurig je, huftalen jb, bradner wt. experimental antitumor activity and toxicity of a new chemotherapeutic agent, bbm 928a. cancer res. 1983 apr;43(4):1504-10.
Check Digit Verification of cas no
The CAS Registry Mumber 75580-37-9 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 7,5,5,8 and 0 respectively; the second part has 2 digits, 3 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 75580-37:
(7*7)+(6*5)+(5*5)+(4*8)+(3*0)+(2*3)+(1*7)=149
149 % 10 = 9
So 75580-37-9 is a valid CAS Registry Number.
75580-37-9Relevant articles and documents
Total synthesis and comparative evaluation of luzopeptin A - C and quinoxapeptin A - C
Boger, Dale L.,Ledeboer, Mark W.,Kume, Masaharu,Searcey, Mark,Qing, Jin
, p. 11375 - 11383 (2007/10/03)
Full details of the total syntheses of luzopeptin A - C and quinoxapeptin A - C, C2-symmetric cyclic depsidecapeptides bearing two pendant heterocyclic chromophores, are disclosed and serve to establish the quinoxapeptin relative and absolute configuration. Key elements of the approach include the late-stage introduction of the chromophore and penultimate L-Htp acylation permitting the divergent synthesis of the luzopeptins, quinoxapeptins, and structural analogues from a common advanced intermediate. Symmetrical pentadepsipeptide coupling and macrocyclization of the 32-membered ring conducted at the single secondary amide site provided the common cyclic decadepsipeptide. The convergent preparation of the required pentadepsipeptide with installation of the labile ester in the final coupling was achieved under surprisingly effective racemization-free conditions. The quinoxapeptins were shown to bind to DNA by high-affinity bisintercalation analogous to sandramycin and the luzopeptins. Significant similarities in the DNA binding of sandramycin and luzopeptin A were observed, and these compounds proved distinguishable from the quinoxapeptins, indicating that the structural alterations in the chromophore impact the affinity and selectivity more than the changes in the decadepsipeptide. The luzopeptins proved to be more potent cytotoxic agents than the corresponding quinoxapeptin, but the quinoxapeptins proved to be more potent inhibitors of HIV-1 reverse transcriptase. In addition, a well-defined potency order was observed in the cytotoxic assays (A > B > C) in which the distinctions were extraordinarily large, with the removal of each L-Htp acyl substituent resulting in a 100-1000-fold reduction in potency. An equally well-defined but reverse potency order was observed in HIV-1 reverse transcriptase inhibition (C > B > A). Thus, the non-naturally occurring synthetic precursor 6 (quinoxapeptin C) was found to exhibit the most potent HIV-1 reverse transcriptase inhibition in the series and to lack a dose-limiting in vitro cytotoxic activity, making it the most attractive member of the series examined.
