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Fig. 1 · Structure
Cat. No.
A10106
CAS No.
37318-06-2
Formula
C54H88O18
Mol. Weight
1025.3

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Elaiophylin (Azalomycin-B)

Cat. No. A10106 CAS 37318-06-2

Azalomycin-B is a macrolide antibiotic produced by Streptomyces hygroscopicus.

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Biological Activity

Bioactivity / Mechanism

Elaiophylin has been studied as a late-stage autophagy inhibitor. In SKOV3 cells, it increased LC3B/SQSTM1 accumulation while reducing lysosomal proteolysis and cathepsin B/D activity. Colocalization experiments supported preserved autophagosome–lysosome fusion. These cellular findings do not establish direct inhibition of purified cathepsins. [1]

Elaiophylin disrupted Hsp90/Cdc37 interaction in lysate-based assays, with reported IC50 values of 14 ± 5 µM for full-length Hsp90 and 11 ± 4 µM for its N-terminal domain (mean ± SEM). At 10 µM it did not displace an ATP-pocket probe. This supports an interaction-disrupting mechanism under the tested conditions. [2]

A later study reported SHP2 binding by surface plasmon resonance (KD 3.702 μM). In SKOV3 cells, SHP2 knockdown partially reversed elaiophylin-associated loss of lysosomal dye signal and cathepsin activity. The authors interpreted these findings within a paraptosis-associated mechanism of autophagy impairment; SHP2 binding alone does not establish enzymatic activation or a single exclusive target. [3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cellular Effect

Cell Line Activity Value Description Reference
DU-145 IC50 31 nM Cytotoxicity against human DU145 cells assessed as reduction in cell viability incubated for 24 hrs by FMCA method [PMID: 31079965]
HEK293 IC50 0.2 μM Cytotoxicity against HEK293 cells assessed as reduction in cell viability incubated for 24 hrs by FMCA method [PMID: 31079965]
Huh-7 IC50 4.2 nM Cytotoxicity against human HuH7 cells assessed as reduction in cell viability incubated for 24 hrs by FMCA method [PMID: 31079965]

In Vitro Studies

After 72 h, elaiophylin reduced alamarBlue readouts in MDA-MB-231 and MIA PaCa-2 cultures, with IC50 values of 0.37 and 0.26 μM in 2D and 0.36 and 0.31 μM in preformed 3D spheres, respectively. The experiment used two independent biological repeats. These assay-specific potencies are not recommended treatment concentrations. [2]

Autophagic flux and lysosomal function in SKOV3 cells

Cell-based study · SKOV3 ovarian cancer cells, including GFP-LC3B-expressing cells [1]

Elaiophylin increased LC3B/SQSTM1 accumulation and reduced lysosomal proteolysis and cathepsin activity. Chloroquine did not significantly add to the GFP-LC3B puncta response, supporting impaired late-stage flux. Colocalization experiments did not support a block in autophagosome–lysosome fusion.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
GFP-LC3B puncta after chloroquine addition to elaiophylincomparison No significant additional increase[1]
CTSB and CTSD activity following cellular exposuredirection Both decreased with time[1]
GFP-LC3B/LAMP1-RFP overlapPearson correlation coefficient 0.59 ± 0.09[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.5 μM
Exposure duration
12 h for flux/colocalization and DQ-BSA; 6, 12 and 24 h for cathepsin activity
Method
Cellular exposure followed by fluorescence imaging, immunoblotting and lysosomal activity readouts
Vehicle
DMSO control; final fraction not stated in the selected assay descriptions
Co-treatment
Mechanistic comparator arms: 3-MA (10 mM), chloroquine (25 μM); starvation (EBSS) comparator for fusion. These are distinct from elaiophylin alone.
Reported limits
No direct purified-cathepsin binding or inhibition assay establishes cathepsins as the molecular target. Exact bar values were not reconstructed.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Figures 2A–E, 3A–D, 4B–C; corresponding Results; Reagents and antibodies; Cathepsin activity assay

GFP-LC3B puncta after chloroquine addition to elaiophylin: Fluorescence microscopy; triplicate samples, at least 100 cells/sample; mean ± SEM — Figure 2A–C and legend; Results: Autophagic flux was inhibited by elaiophylin treatment

CTSB and CTSD activity following cellular exposure: Fluorogenic substrate assays of treated-cell material; mean ± SD, 3 independent experiments — Figure 4C and legend; Cathepsin activity assay methods

GFP-LC3B/LAMP1-RFP overlap: Confocal microscopy; mean ± SD; >30 cells per condition, representative of 3 independent experiments — Figure 3A image and legend

Hsp90/Cdc37 interaction disruption and ATP-pocket control

Biochemical assay · HEK293 lysate-based split Renilla luciferase Hsp90/Cdc37 assays; Hsp90α N-terminal fluorescence-polarization competition assay [2]

Elaiophylin reduced Hsp90/Cdc37 interaction signals in both full-length and N-terminal configurations. It did not displace fluorescent geldanamycin at the tested concentration.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Full-length Hsp90/Cdc37 interaction signalIC50 14 ± 5 µM[2]
N-terminal Hsp90/Cdc37 interaction signalIC50 11 ± 4 µM[2]
Competition with fluorescent geldanamycin for Hsp90 ATP-pocketcompetition No displacement detected at 10 μM[2]

Literature-Reported Treatment Conditions

Treatment concentration
Increasing concentrations for interaction assays (complete series not tabulated); 10 μM in ATP-pocket comparison
Exposure duration
Split assay: sequential 5 min and 2 min incubations before substrate/readout; competition assay: 2 h
Method
Cell-lysate interaction assays and fluorescence-polarization competition
Vehicle
0.1% DMSO control in split assay
Co-treatment
No combination treatment; comparators tested separately
Reported limits
Biological n for Figure 1C–E not specified in its legend; concentration series not converted from graph axes.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Sections 2.1, 2.5, 2.6, 2.12 and 3.1; Figure 1C–E

Full-length Hsp90/Cdc37 interaction signal: Lysate-based split Renilla luciferase; mean ± SEM per section 2.12; n not specified for this panel — Section 3.1, Figure 1C; sections 2.5 and 2.12

N-terminal Hsp90/Cdc37 interaction signal: Lysate-based split Renilla luciferase; mean ± SEM per section 2.12; n not specified for this panel — Section 3.1, Figure 1D; sections 2.5 and 2.12

Competition with fluorescent geldanamycin for Hsp90 ATP-pocket: Fluorescence polarization; 17-AAG, geldanamycin and luminespib positive comparators; samples analyzed in triplicate — Figure 1E and legend; sections 2.6 and 3.1

Comparative 2D and 3D growth responses

Cell-based study · MDA-MB-231 breast cancer and MIA PaCa-2 pancreatic cancer cells in 2D cultures and preformed 3D tumorospheres [2]

Elaiophylin reduced the alamarBlue readout in both culture formats after 72 h. The reported IC50 values were submicromolar in both cell lines.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
MDA-MB-231 2D viability/proliferation readoutIC50 0.37 μM[2]
MIA PaCa-2 2D viability/proliferation readoutIC50 0.26 μM[2]
MDA-MB-231 3D tumorosphere readoutIC50 0.36 μM[2]
MIA PaCa-2 3D tumorosphere readoutIC50 0.31 μM[2]

Literature-Reported Treatment Conditions

Treatment concentration
2D: 1:2 serial dilution starting at 2 μM. Complete 3D treatment series not tabulated; illustrated conditions include 0.3125 and 1.25 μM.
Exposure duration
72 h treatment
Method
alamarBlue fluorescence in monolayers and preformed spheres
Vehicle
0.1% DMSO in 2D; 3D method adds a 0.3% DMSO solution to existing medium (final fraction not explicitly stated)
Co-treatment
Single-agent elaiophylin
Reported limits
No uncertainty intervals for fitted IC50 values. Sphere assay measures response of preformed spheres, not de novo sphere initiation.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Figure 3A–B; sections 2.1, 2.7, 2.8, 2.12 and 3.3

MDA-MB-231 2D viability/proliferation readout: alamarBlue; n = 2 independent biological repeats; plotted data mean ± SEM — Figure 3A image/legend; sections 2.8 and 2.12

MIA PaCa-2 2D viability/proliferation readout: alamarBlue; n = 2 independent biological repeats; plotted data mean ± SEM — Figure 3A image/legend; sections 2.8 and 2.12

MDA-MB-231 3D tumorosphere readout: alamarBlue after treating 6-day preformed spheres; n = 2; plotted data mean ± SEM — Figure 3B image/legend; sections 2.7 and 2.12

MIA PaCa-2 3D tumorosphere readout: alamarBlue after treating 6-day preformed spheres; n = 2; plotted data mean ± SEM — Figure 3B image/legend; sections 2.7 and 2.12

Direct interaction with recombinant SHP2

Biochemical assay · Human recombinant SHP2 immobilized on a CM5 sensor [3]

Surface plasmon resonance supported direct interaction between elaiophylin and recombinant SHP2.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Binding to human recombinant SHP2KD 3.702 μM[3]

Literature-Reported Treatment Conditions

Treatment concentration
Maximum 60 µM with five additional concentrations in a 3-fold dilution series
Exposure duration
Equilibrium binding analysis; contact duration not specified
Method
Surface plasmon resonance
Vehicle
Running buffer: 20 mM HEPES pH 7.4, 150 mM NaCl, 0.05% surfactant P20
Co-treatment
Single analyte; no combination
Reported limits
Replicate n, uncertainty interval, reference-channel details and association/dissociation rate constants not reported in the selected SPR description.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Figure 4d; Results: CRISPR library screening identifies PTPN11; Surface plasmon resonance assay; Compounds and antibodies

Binding to human recombinant SHP2: Surface plasmon resonance; steady-state affinity fit at equilibrium, 25 °C — Figure 4d image; Surface plasmon resonance (SPR) assay methods

SHP2 knockdown attenuates lysosomal effects

Cell-based study · SKOV3 cells with control siRNA or two independent PTPN11-directed siRNAs [3]

PTPN11 knockdown partially restored LysoTracker signal and cathepsin B/D activity after elaiophylin exposure, linking SHP2 to the lysosomal phenotype.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
LysoTracker Deep Red signaldirection Partial restoration after PTPN11 knockdown[3]
CTSB and CTSD activitydirection Partial restoration after PTPN11 knockdown[3]

Literature-Reported Treatment Conditions

Treatment concentration
0.5 µM
Exposure duration
24 h for LysoTracker; 36 h for cathepsin activity
Method
Elaiophylin exposure following control or PTPN11 siRNA; lysosomal readouts
Vehicle
Exact final vehicle fraction not specified for these panels
Co-treatment
Genetic perturbation, not drug combination; control siRNA and corresponding unexposed groups included
Reported limits
No exact fluorescence/activity effect sizes reconstructed from plotted bars.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Figure 5d–e and 5h–i; Results: Elaiophylin-induced paraptosis blocks autophagy by impairing lysosomal function; siRNA and plasmid; Cathepsin activity assay

LysoTracker Deep Red signal: Flow cytometry; mean ± SD, three independent experiments; two-tailed unpaired Student t test — Figure 5d–e and legend

CTSB and CTSD activity: Activity assays of cell lysates; mean ± SD, three independent experiments; two-tailed unpaired Student t test — Figure 5h–i and legend; Cathepsin activity assay methods

In Vivo Studies

In an orthotopic ovarian tumor model, elaiophylin at 2 mg/kg intraperitoneally every 2 days reduced primary tumor volume by ∼60% and reduced mesenteric metastases versus DMSO control (n = 8 per cohort; P < 0.05 for both endpoints). This is preclinical efficacy evidence, not a pharmacokinetic study. [1]

The same report described toxicity at a different regimen: 8 mg/kg intraperitoneally daily caused weight loss in 6/8 mice, lethargy with arched backs in 4/8, and bowel obstruction in 6/8. The lower-dose tumor findings therefore do not establish general tolerability or a clinical therapeutic window. [1]

Orthotopic ovarian tumor growth and metastasis

Animal study · Female NOD/SCID mice bearing orthotopic GFP-LC3B-SKOV3 ovarian tumors; n = 8 per cohort [1]

Elaiophylin monotherapy reduced primary ovarian tumor volume and mesenteric metastases compared with DMSO control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Primary ovarian tumor volumerelative reduction ∼60%; P < 0.05 versus DMSO[1]
Mesenteric metastasescomparison Fewer metastases; P < 0.05 versus DMSO[1]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Every 2 d
Treatment course
Began 1 week after implantation; necropsy at 8 weeks after implantation
Vehicle
DMSO control named; full administration formulation not specified
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Elaiophylin monotherapy
2 mg/kg		DMSO-treated tumor-bearing cohort∼60% reduction in primary tumor volume; fewer mesenteric metastases (both P < 0.05 versus DMSO)[1]
Elaiophylin monotherapy
Model: Female NOD/SCID mice with orthotopic GFP-LC3B-SKOV3 ovarian tumors; 8 mice per cohort
Reported limits: Injection volume and complete formulation not specified. Exact metastasis counts not transcribed from bars.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published results for the named compound in the specified model; not a validation of an Adooq lot.

Figure 7E–H; adjacent Results; Orthotopic model methods

Primary ovarian tumor volume: Tumor volume assessment; blinded investigators per orthotopic methods; n = 8 per cohort — Figure 7E–F and legend; adjacent Results paragraph; Orthotopic model methods

Mesenteric metastases: Lesion assessment at necropsy; n = 8 per cohort — Figure 7G–H and legend; adjacent Results paragraph

Elaiophylin monotherapy · Figure 7E–H; adjacent orthotopic Results paragraph; Orthotopic model methods

Higher-dose elaiophylin toxicity in orthotopic ovarian xenograft-bearing mice

Animal study · Mice bearing SKOV3 orthotopic ovarian cancer xenografts; 8 mg/kg group denominators reported as 8 mice; regimen-specific strain, sex and age not specified in the toxicity paragraph [1]

At the separately described 8 mg/kg intraperitoneal daily regimen, the main text reports weight loss in 6/8 mice, lethargy with arched backs in 4/8 and bowel obstruction in 6/8. These observations do not establish general tolerability or a clinical therapeutic window.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Weight lossobserved count 6/8 mice[1]
Lethargy with arched backsobserved count 4/8 mice[1]
Bowel obstructionobserved count 6/8 mice[1]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Daily
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
8 mg/kg daily toxicity observations
8 mg/kg		DMSO comparator named in toxicity paragraph; group size and event counts not supplied thereWeight loss in 6/8 mice; lethargy with arched backs in 4/8; bowel obstruction in 6/8[1]
8 mg/kg daily toxicity observations
Model: Mice bearing SKOV3 orthotopic ovarian cancer xenografts; event denominators 8
Reported limits: Toxicity-specific course/start/end, escalation sequence and whether the dose groups used distinct animals, mouse strain/sex/age for this regimen, vehicle formulation/injection volume, control-group size/counts, ascertainment criteria and statistical analysis are not specified in this main-text paragraph. SI not retrieved; no histologic verification. Do not transfer lower-dose efficacy methods.
Methods and source locations

Compound reported in the paper: Elaiophylin

Published observations for the named compound and regimen; not an Adooq lot validation or clinical safety assessment.

Results: Elaiophylin exerted autophagy inhibition and antitumor efficacy in vivo; paragraph beginning “To determine whether higher elaiophylin doses” (main-text reports; cites Figures S10–S11, not inspected)

Weight loss: Descriptive toxicity observation reported in original main-text Results; ascertainment criteria and observation interval unspecified; no supplementary histology inspected — Results: Elaiophylin exerted autophagy inhibition and antitumor efficacy in vivo; paragraph beginning “To determine whether higher elaiophylin doses” (main-text reports; cites Figures S10–S11, not inspected)

Lethargy with arched backs: Descriptive toxicity observation reported in original main-text Results; ascertainment criteria and observation interval unspecified; no supplementary histology inspected — Results: Elaiophylin exerted autophagy inhibition and antitumor efficacy in vivo; paragraph beginning “To determine whether higher elaiophylin doses” (main-text reports; cites Figures S10–S11, not inspected)

Bowel obstruction: Descriptive toxicity observation reported in original main-text Results; ascertainment criteria and observation interval unspecified; no supplementary histology inspected — Results: Elaiophylin exerted autophagy inhibition and antitumor efficacy in vivo; paragraph beginning “To determine whether higher elaiophylin doses” (main-text reports; cites Figures S10–S11, not inspected)

8 mg/kg daily toxicity observations · Results: Elaiophylin exerted autophagy inhibition and antitumor efficacy in vivo; paragraph beginning “To determine whether higher elaiophylin doses” (main-text reports; cites Figures S10–S11, not inspected)

Specifications

Manufacturer Adooq Bioscience
CAS Number 37318-06-2
Formula C54H88O18
Molecular Weight 1025.3
Synonyms Salbomycin; Gopalamicin; SNA 4606-3; Azalomycin-B
SMILES
CC[C@H]1[C@@H](C[C@](O[C@@H]1C)(O)[C@H]([C@H](O)[C@@H]([C@H]2OC(=O)/C=C/C=C/[C@@H]([C@H](OC(=O)/C=C/C=C/[C@@H]2C)[C@H]([C@@H](O)[C@@H]([C@@]3(O[C@@H]([C@H]([C@@H](C3)O[C@@H]4O[C@H]([C@H]([C@H](C4)O)O)C)CC)C)O)C)C)C)C)C)O[C@@H]5O[C@H]([C@H]([C@H](C5)O)O)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Zhao X, Fang Y, Yang Y, et al. Elaiophylin, a novel autophagy inhibitor, exerts antitumor activity as a single agent in ovarian cancer cells. Autophagy (2015). PMID: 25893854 DOI: 10.1080/15548627.2015.1017185 Source material
  2. [2] Siddiqui FA, Vukic V, Salminen TA, et al. Elaiophylin Is a Potent Hsp90/ Cdc37 Protein Interface Inhibitor with K-Ras Nanocluster Selectivity. Biomolecules (2021). PMID: 34199986 DOI: 10.3390/biom11060836 Source material
  3. [3] Li GN, Zhao XJ, Wang Z, et al. Elaiophylin triggers paraptosis and preferentially kills ovarian cancer drug-resistant cells by inducing MAPK hyperactivation. Signal transduction and targeted therapy (2022). PMID: 36097006 DOI: 10.1038/s41392-022-01131-7 Source material

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