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Fig. 1 · Structure
Cat. No.
A11478
CAS No.
1062368-62-0
Formula
C25H22N6.HCl
Mol. Weight
442.94

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LDN193189 HCl

Cat. No. A11478 CAS 1062368-62-0
LDN193189 HCl is the hydrochloride salt of LDN193189. LDN193189 is a highly potent small molecule BMP inhibitor that inhibits BMP type I receptors ALK2 (IC50: 5 nM), ALK3 (IC50: 30 nM) and ALK6 (TGFβ1/BMP signaling) and subsequent SMAD phosphorylation.

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Publications for LDN193189 HCl

2 publications citing this product

  1. Andreea Manole, .et al. , Cell Rep, 2023, Dec 26;42(12):113466 PMID: 38039131
  2. Brandon J.Peiffer, .et al. , Cell Chem Biol, 2019, 26, 1-10 PMID: 30827938
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Biological Activity

Target & Activity

Target Activity Value
ALK2 (C2C12 cells) 5 nM
ALK3 (C2C12 cells) 30 nM

In Vitro Studies

Peiffer et al. identified Adooq A11478 in their resource table. In Jurkat cells, 100 nM LDN-193189 suppressed BMP-responsive reporter induction by FK506, FKVP or BMP4 after 18 h. This experiment used LDN as a pathway-inhibition control. [1]

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

A11478 suppresses induced BMP reporter activity

Cell-based study · Human Jurkat E6.1 T cells transfected with BRE-Luc [1]

LDN blocked BMP-responsive reporter induction by FK506 or FKVP and by BMP4. This is an inhibitor control within a BMP-activation experiment.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
ID1-promoter/BRE-luciferase inductionReporter response 100 nM LDN suppressed reporter induction by 1 µM FK506, 1 µM FKVP or 50 ng/ml BMP4.[1]

Literature-Reported Treatment Conditions

Treatment concentration
100 nM LDN
Exposure duration
18 h
Method
BRE-luciferase reporter
Vehicle
DMSO-normalized control; compound/protein stock addition described in RPMI with 0.5% DMSO
Co-treatment
Separate combinations with FK506 1 µM, FKVP 1 µM or BMP4 50 ng/ml
Reported limits
Final DMSO percentage for Figure 3A is not explicitly assigned. Replicate wells are not independent biological experiments.
Methods and source locations

Compound reported in the paper: LDN-193189; Compound label in the paper: LDN

Adooq A11478 research use; no lot purity, salt-stoichiometry or equivalence certification.

Figure 3A; reporter Methods; Key Resources Table; Quantification: In Vitro Statistics

ID1-promoter/BRE-luciferase induction: 18 h reporter exposure; background-subtracted luminescence normalized to DMSO control; n = 3 replicate wells; error bars SD. BMP4 positive, TGF-beta1 negative and cyclosporine A comparator controls. — Figure 3A image/caption; Results: FKVP activates ID-1 reporter; Methods: BMP and NFAT Pathway Reporters; Key Resources Table; In Vitro Statistics

In Vivo Studies

In diabetic Goto-Kakizaki rats, Adooq A11478 (LDN-193189, 2 mg/kg/day intraperitoneally) delayed complete wound healing during AMD3100/FK506 combination treatment from 21 to 25 days, as reported in the Results. LDN alone did not significantly alter healing relative to saline. The result concerns reversal of a combination response. [1]

A11478 reverses accelerated healing under AF combination therapy

Animal study · Diabetic Goto-Kakizaki rats; four wounds per animal [1]

Systemic LDN delayed complete re-epithelialization under AMD3100/FK506 treatment, while LDN alone did not significantly alter healing relative to saline. This demonstrates reversal of a combination response, not a pro-healing LDN effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Time to complete re-epithelializationDays to complete healing AF: 21 days; AF + LDN: 25 days (rounded Results values); AF vs AF + LDN p = 0.000509; saline vs saline + LDN p = 0.806.[1]
CD133-positive staining in wound granulation tissueQualitative immunohistochemistry Less CD133-positive staining with AF + LDN than with AF alone at day 7.[1]

Conditions shared by the study groups

Treatment course
AF/saline begins immediately after wounding and continues until complete healing; LDN given with these regimens.
Vehicle
Saline control; LDN formulation not specified in read animal method
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Saline control (n = 10 rats)—Reference wound-healing group.[1]
Saline + LDN (n = 3 rats)
LDN 2 mg/kg/day		Saline aloneNo significant healing-time difference from saline; Figure 5B p = 0.806.[1]
AF combination (n = 10 rats)
AMD3100 1 mg/kg + FK506 0.1 mg/kg		SalineComplete healing at 21 days as rounded in Results.[1]
AF + LDN (n = 6 rats)
LDN 2 mg/kg/day + AMD3100 1 mg/kg + FK506 0.1 mg/kg		AF aloneHealing delayed from 21 to 25 days as rounded in Results; Figure 5B p = 0.000509 versus AF. Reduced CD133 staining shown at day 7.[1]
Saline control (n = 10 rats)
Model: Diabetic Goto-Kakizaki rats; four wounds measured per rat
Route: Subcutaneous
Frequency: Every other day
Reported limits: Sex allocation and LDN formulation for this cohort are not specified in the read wound method.
Saline + LDN (n = 3 rats)
Model: Diabetic Goto-Kakizaki rats; four wounds measured per rat
Route: LDN intraperitoneal; saline subcutaneous
Frequency: LDN daily; saline every other day
Reported limits: Sex allocation and LDN formulation for this cohort are not specified in the read wound method.
AF combination (n = 10 rats)
Model: Diabetic Goto-Kakizaki rats; four wounds measured per rat
Route: Subcutaneous
Frequency: Every other day
Reported limits: Sex allocation and LDN formulation for this cohort are not specified in the read wound method.
AF + LDN (n = 6 rats)
Model: Diabetic Goto-Kakizaki rats; four wounds measured per rat
Route: LDN intraperitoneal; AF subcutaneous
Frequency: LDN daily; AF every other day
Reported limits: Sex allocation and LDN formulation for this cohort are not specified in the read wound method.
Methods and source locations

Compound reported in the paper: LDN-193189; Compound label in the paper: LDN

Adooq A11478 research use; no lot purity, salt-stoichiometry or equivalence certification.

Figure 5A–C; Results: BMP signaling required for beneficial AF therapy; Methods: In Vivo Excisional Wound Model; In Vivo Statistics

Time to complete re-epithelialization: Figure 5B: mean ± SEM; n refers to rats (saline 10; saline+LDN 3; AF 10; AF+LDN 6). Four wounds per rat measured. One-way ANOVA with Bonferroni-Holm post-hoc adjustment. — Figure 5B image/caption; wound Results; In Vivo Statistics

CD133-positive staining in wound granulation tissue: Representative images, 40×; no numerical cell count or effect size inferred. — Figure 5C image/caption; associated Results

Saline control (n = 10 rats) · Figure 5A–C; Results: BMP signaling required for beneficial AF therapy; Methods: In Vivo Excisional Wound Model; In Vivo Statistics

Saline + LDN (n = 3 rats) · Figure 5A–C; Results: BMP signaling required for beneficial AF therapy; Methods: In Vivo Excisional Wound Model; In Vivo Statistics

AF combination (n = 10 rats) · Figure 5A–C; Results: BMP signaling required for beneficial AF therapy; Methods: In Vivo Excisional Wound Model; In Vivo Statistics

AF + LDN (n = 6 rats) · Figure 5A–C; Results: BMP signaling required for beneficial AF therapy; Methods: In Vivo Excisional Wound Model; In Vivo Statistics

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1062368-62-0
Formula C25H22N6.HCl
Molecular Weight 442.94
Synonyms LDN 193189
SMILES
C1CN(CCN1)C2=CC=C(C=C2)C3=CN4C(=C(C=N4)C5=CC=NC6=CC=CC=C56)N=C3.Cl

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] Peiffer BJ, Qi L, Ahmadi AR, et al. Activation of BMP Signaling by FKBP12 Ligands Synergizes with Inhibition of CXCR4 to Accelerate Wound Healing Cell chemical biology (2019). PMID: 30827938 DOI: 10.1016/j.chembiol.2019.01.011 Source material

Publications

2 publications citing this product

  1. Andreea Manole, .et al. , Cell Rep, 2023, Dec 26;42(12):113466 PMID: 38039131
  2. Brandon J.Peiffer, .et al. , Cell Chem Biol, 2019, 26, 1-10 PMID: 30827938

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