webinar
Oct. 27-28, 2025, Boston, MA, USA - Booth 114.
Read More

Mytoxin B

  CAS No.: 105049-15-8   Cat No.: BADC-00809   Purity: ≥95% 4.5  

Mytoxin B is a satratoxin-type trichothecene macrolide and is similar to the effect of LY294002. Mytoxin B induces cell apoptosis via PI3K/Akt pathway. An ADC cytotoxin.

Mytoxin B

Structure of 105049-15-8

Quality
Assurance

Worldwide
Delivery

24/7 Customer
Support
Category
ADC Cytotoxin
Molecular Formula
C29H36O9
Molecular Weight
528.59
Target
PI3K/Akt Pathway
Shipping
Room temperature
Shipping
-20°C

* For research and manufacturing use only. We do not sell to patients.

Size Price Stock Quantity
-- $-- In stock

Looking for different specifications? Click to request a custom quote!

Capabilities & Facilities

Popular Publications Citing BOC Sciences Products
Synonyms
mytoxin B; 105049-15-8; (1'Z,2S,6'R,11'R,13'R,15'S,16'R,19'Z,23'R,27'R)-23'-acetyl-27'-hydroxy-9',15'-dimethyl-4',12',17',24'-tetraoxaspiro[oxirane-2,14'-pentacyclo[21.3.1.1,.0,.0,octacosane]-1',9',19'-triene-3',18'-dione
IUPAC Name
(1Z,6R,11R,13R,14S,15S,16R,19E,23R,27R)-23-acetyl-27-hydroxy-9,15-dimethylspiro[4,12,17,24-tetraoxapentacyclo[21.3.1.113,16.06,11.06,15]octacosa-1,9,19-triene-14,2'-oxirane]-3,18-dione
Canonical SMILES
CC1=CC2C3(CC1)COC(=O)C=C4CCOC(C4O)(CCC=CC(=O)OC5C3(C6(CO6)C(C5)O2)C)C(=O)C
InChI
InChI=1S/C29H36O9/c1-17-7-10-27-15-34-24(32)13-19-8-11-35-28(18(2)30,25(19)33)9-5-4-6-23(31)38-20-14-22(37-21(27)12-17)29(16-36-29)26(20,27)3/h4,6,12-13,20-22,25,33H,5,7-11,14-16H2,1-3H3/b6-4+,19-13-/t20-,21-,22-,25-,26-,27-,28+,29+/m1/s1
InChIKey
LXIQXFWXXPJPEE-OICCJBEUSA-N
Solubility
DMSO: 15 mg/ml (ultrasonic, warming)
PSA
120.89000
Appearance
Solid Power
Shelf Life
≥ 2 years
Shipping
Room temperature
Storage
-20°C
In Vivo
MTT assay showed that mytoxin B and myrothecine A inhibited the proliferation of SMMC-7721 cells in dose- and time-dependent manners. Annexin V-FITC/PI dual staining assay revealed that mytoxin B and myrothecine A both could induce SMMC-7721 cells apoptosis in a dose-dependent manner. The decreased expression level of anti-apoptotic protein Bcl-2 and the increased expression level of pro-apoptotic protein Bax were observed apparently in Western blot analysis. The reduced ratio of Bcl-2/Bax further confirmed the apoptosis-inducing effect of mytoxin B and myrothecine A on SMMC-7721 cells. Moreover, the expression levels of caspases-3, -8, and -9, and cleaved caspases-3, -8, and -9 were all upregulated in both mytoxin B and myrothecine A-treated cells in Western blot analysis, which indicated that both compounds might induce SMMC-7721 cells apoptosis through not only the death receptor pathway but also the mitochondrial pathway. Finally, mytoxin B and myrothecine A were found to reduce the activity of PI3K/Akt signaling pathway that was similar to the effect of LY294002 (a potent and specific PI3K inhibitor), suggesting that both mytoxin B and myrothecine A might induce SMMC-7721 cells apoptosis via PI3K/Akt pathway.
1. Two Trichothecene Mycotoxins from Myrothecium roridum Induce Apoptosis of HepG-2 Cells via Caspase Activation and Disruption of Mitochondrial Membrane Potential
Weimin Zhang, Zhanghua Sun, Hongxin Liu, Saini Li, Yuchan Chen, Wei Ye, Haohua Li, Taomei Liu Molecules . 2016 Jun 17;21(6):781. doi: 10.3390/molecules21060781.
Trichothecene mycotoxins are a type of sesquiterpenoid produced by various kinds of plantpathogenic fungi. In this study, two trichothecene toxins, namely, a novel cytotoxic epiroridin acid and a known trichothecene, mytoxin B, were isolated from the endophytic fungus Myrothecium roridum derived from the medicinal plant Pogostemon cablin. The two trichothecene mytoxins were confirmed to induce the apoptosis of HepG-2 cells by cytomorphology inspection, DNA fragmentation detection, and flow cytometry assay. The cytotoxic mechanisms of the two mycotoxins were investigated by quantitative real time polymerase chain reaction, western blot, and detection of mitochondrial membrane potential. The results showed that the two trichothecene mycotoxins induced the apoptosis of cancer cell HepG-2 via activation of caspase-9 and caspase-3, up-regulation of bax gene expression, down-regulation of bcl-2 gene expression, and disruption of the mitochondrial membrane potential of the HepG-2 cell. This study is the first to report on the cytotoxic mechanism of trichothecene mycotoxins from M. roridum. This study provides new clues for the development of attenuated trichothecene toxins in future treatment of liver cancer.
2. Mytoxin B and Myrothecine A Induce Apoptosis in Human Hepatocarcinoma Cell Line SMMC-7721 via PI3K/Akt Signaling Pathway
Fengwei Lyu, Yi Fu, Lijun Liu, Huiliang Song, Dan Wan, Li Shen, Wenjing Xia Molecules . 2019 Jun 20;24(12):2291. doi: 10.3390/molecules24122291.
Trichothecene macrolides comprise a class of valuable leading compounds in developing anticancer drugs, however, there are few reports concerning their anticancer mechanisms, especially the anticancer mechanism of the 10,13-cyclotrichothecane derivatives that are found mainly in symbiotic fungi. In vitro anticancer activity of two trichothecene macrolides mytoxin B and myrothecine A against the human hepatocarcinoma cell line SMMC-7721 was investigated in the present study. MTT assay showed that mytoxin B and myrothecine A inhibited the proliferation of SMMC-7721 cells in dose- and time-dependent manners. Annexin V-FITC/PI dual staining assay revealed that mytoxin B and myrothecine A both could induce SMMC-7721 cells apoptosis in a dose-dependent manner. The decreased expression level of anti-apoptotic protein Bcl-2 and the increased expression level of pro-apoptotic protein Bax were observed apparently in Western blot analysis. The reduced ratio of Bcl-2/Bax further confirmed the apoptosis-inducing effect of mytoxin B and myrothecine A on SMMC-7721 cells. Moreover, the expression levels of caspases-3, -8, and -9, and cleaved caspases-3, -8, and -9 were all upregulated in both mytoxin B and myrothecine A-treated cells in Western blot analysis, which indicated that both compounds might induce SMMC-7721 cells apoptosis through not only the death receptor pathway but also the mitochondrial pathway. Finally, mytoxin B and myrothecine A were found to reduce the activity of PI3K/Akt signaling pathway that was similar to the effect of LY294002 (a potent and specific PI3K inhibitor), suggesting that both mytoxin B and myrothecine A might induce SMMC-7721 cells apoptosis via PI3K/Akt pathway.
3. Cytotoxic trichothecene macrolides from the endophyte fungus Myrothecium roridum
Hong-Xin Liu, Zhang-Hua Sun, Yu-Zhi Tan, Yu-Chan Chen, Hao-Hua Li, Wei-Min Zhang, Wei-Zhen Liu J Asian Nat Prod Res . 2016 Jul;18(7):684-9. doi: 10.1080/10286020.2015.1134505.
A new cytotoxic roridin-type trichothecene macrolide named epiroridin acid (1) and two known compounds epiroridin E (2) and mytoxin B (3) were isolated from the liquid culture of Myrothecium roridum A553, which was isolated from the medicinal plant Pogostemon cablin. The structure of the new macrolide (1) was elucidated by extensive spectroscopic measurements (UV, IR, MS, and 1D and 2D NMR) analyses. All isolated compounds (1-3) were evaluated for their cytotoxic activities against SF-268, MCF-7, NCI-H460, and HepG-2 tumor cell lines. The new compound (1) exhibited well cytotoxicity against the four selected tumor cell lines.

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Related Products

Contact our experts today for pricing and comprehensive details on our ADC offerings.

You May Also Be Interested In

From cytotoxin synthesis to linker design, discover our specialized services that complement your ADC projects.

ADC Payload Development Biological Payload Chemical Payload Protein Toxin Nanocarrier Microtubule Inhibitors DNA Damaging Agents RNA Polymerase Inhibitors Protein Degraders

Unlock Deeper ADC Insights

Learn more about payload design, linker strategies, and integrated CDMO support through our curated ADC content.

Maytansine and Its Analogues Cytotoxic Agents Used in Antibody–Drug Conjugates Exatecan Mesylate in ADCs: A New Topo I Inhibitor What is Calicheamicin? What is Monomethyl Auristatin E (MMAE)? What is Monomethyl Auristatin F (MMAF)? What is Pyrrolobenzodiazepine (PBD)? Antiviral Potential of Thapsigargin in COVID-19 Research ADC Payloads Explained: Current Types and Cutting-Edge Research Progress Tubulin Inhibitors - Highly Potential ADC Payloads

Explore More ADC Products

Find exactly what your project needs from our expanded range of ADCs, offering flexible options to fit your timelines and goals.

ADC Cytotoxin

Powerful Targeted Cancer Solutions

ADC  Cytotoxin with Linker

Enhanced Stability And Efficacy

ADC Linker

Precise Conjugation For Success

Antibody-Drug  Conjugates (ADCs)

Maximized Therapeutic Performance

Auristatins

Next-Level Tubulin Inhibition

Calicheamicins

High-Impact DNA Targeting

Camptothecins

Advanced Topoisomerase Inhibition

Daunorubicins / Doxorubicins

Trusted Anthracycline Payloads

Duocarmycins

Potent DNA Alkylation Agents

Maytansinoids

Superior Microtubule Disruption

Pyrrolobenzodiazepines

Ultra-Potent DNA Crosslinkers

Traditional Cytotoxic Agents

Proven Chemotherapy Solutions

Cleavable Linker

Precise Intracellular Drug Release

Non-Cleavable Linker

Exceptional Long-Term Stability

Historical Records: Thailanstatin C | [Tyr2] Scyllatoxin | Duocarmycin DM | Adaphotris | Seco-DuocarmycinDMA | Q Pr | MC-Val-Cit-PAB-duocarmycin | Thailanstatin B | Esperamicin | Quireston-A | Mytoxin B
Send Inquiry
Verification code
Inquiry Basket