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| 1mg |
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| 5mg |
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| Targets |
Galipin receptors (GAL1, GAL2, GAL3). Galantide is a reversible and non-specific galanin receptor antagonist that binds to galanin receptor subtypes GAL1, GAL2, and GAL3 (G protein-coupled receptors). Galanin is a neuropeptide involved in a wide range of physiological functions, including pain modulation, feeding behavior, cognition, mood, neuroendocrine secretion, and neuronal development. Galantide competitively blocks the binding of galanin to its receptors, thereby antagonizing galanin-induced intracellular signaling. At the molecular level, galantide inhibits galanin-evoked G protein-gated inwardly rectifying K+ channel (GIRK) activation, leading to reduced K+ conductance and altered neuronal excitability. Galantide also suppresses voltage-dependent Ba2+ currents (which reflect Ca2+ channel activity). The compound is non-selective among galanin receptor subtypes, making it a broad-spectrum galanin antagonist tool for pharmacologic studies.
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| ln Vitro |
Galantide TFA (0.1-10000 nM) 0.1–10,000 nM) blocks galanin-induced K+ conductance activation with an IC50 value of 4 nM[1]. Galantide TFA (0.1–10,000 nM) has an IC50 value of 16 nM and suppresses voltage-dependent Ba2+ currents in a dose-dependent manner[1]. Regarding voltage-dependent Ba2+ current, the highest inhibition rate of Galantide TFA (0.1–10,000 nM) is almost 40%[1].
In vitro, Galantide TFA is a potent galanin receptor antagonist. In electrophysiological studies using mudpuppy parasympathetic neurons, galantide (0.1-10,000 nM) blocks galanin-induced activation of K+ conductance with an IC50 value of 4 nM, indicating high potency. Galantide (0.1-10,000 nM) also suppresses voltage-dependent Ba2+ currents (a measure of Ca2+ channel activity) in a dose-dependent manner with an IC50 of 16 nM. In receptor binding studies, galantide competitively displaces 125I-galanin from galanin binding sites in rat brain and pancreatic membranes, with Ki values in the low nM range. In CHO cells stably expressing GAL1, GAL2, or GAL3 receptors, galantide antagonizes galanin-induced inhibition of adenylyl cyclase (cAMP accumulation) or activation of phospholipase C (IP3 production) depending on the receptor subtype and cellular context. Galantide inhibits galanin-stimulated food intake and galanin-induced prolactin, growth hormone, and luteinizing hormone (LH) release in cultured pituitary cells and hypothalamic explants. The TFA counterion does not affect antagonist activity. |
| ln Vivo |
In rats with ovariectomies, galantide TFA (5 nm; intracerebroventricular injection, once) suppresses the release of luteinizing hormone caused by ovarian steroids [2]. In ovariectomized rats, the luteinizing hormone spike caused by estradiol benzoate is lessened by galantide TFA (1 and 5 nm; intravenously delivered in three split doses at 1300, 1400, and 1500 hours) [2].
In vivo, galantide (also known as M15 or galantide-15) blocks galanin-mediated physiological responses in several animal models. In rats, intracerebroventricular (i.c.v.) or intrahypothalamic injection of galantide (1-10 nmol) antagonizes galanin-induced feeding behavior (increased food intake) and blocks galanin's inhibitory effect on insulin secretion. Galantide (0.5-2 ug) injected into the paraventricular nucleus (PVN) of the hypothalamus reverses galanin-induced hyperphagia. In the central nervous system, galantide blocks galanin-induced modulation of dopamine and norepinephrine release. In seizure models, galantide may counteract the anticonvulsant effects of galanin, indicating a role of endogenous galanin in seizure suppression. In behavioral models, galantide has been used to investigate the role of galanin in memory, anxiety, and pain perception. Systemic administration (i.v., i.p.) is less effective due to the peptide's poor blood-brain barrier penetration; therefore, central administration (i.c.v., intrathecal) is typically employed. In studies of hormone metabolism, galantide administration in rats blocks galanin-induced inhibition of glucose-stimulated insulin secretion. In models of neurological disorders, galantide is used to dissect the contributions of endogenous galanin signaling. Galantide is not used as a therapeutic and is for research only. |
| Enzyme Assay |
For non-cellular binding assays, a radioligand displacement assay can be performed using membranes prepared from rat brain (hypothalamus, cortex) or from CHO cells expressing recombinant human GAL1, GAL2, or GAL3 receptors. Membranes (10-50 ug protein/well) are incubated with 0.05-0.1 nM 125I-galanin (porcine or human) and varying concentrations of Galantide TFA (0.01-10,000 nM) in binding buffer (50 mM Tris-HCl pH 7.4, 5 mM MgCl2, 0.1% BSA, 0.1% bacitracin, 0.1 mg/mL soybean trypsin inhibitor). After incubation at 25degC for 60-90 minutes, bound and free radioligand are separated by rapid filtration through GF/B glass fiber filters pre-soaked in 0.3% polyethyleneimine using a cell harvester. Filters are washed with cold binding buffer, and filter-bound radioactivity is quantified in a gamma counter. Non-specific binding is determined in the presence of 1 uM unlabeled galanin. IC50 values are converted to Ki using the Cheng-Prusoff equation. The Ki for galantide at galanin receptors typically ranges from 0.1-10 nM depending on the receptor subtype and species. For SPR, purified galanin receptor protein (e.g., GAL2) can be reconstituted in lipid nanodiscs and immobilized on a sensor chip, and galantide at concentrations 0.1-1000 nM is flowed over to determine KD.
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| Cell Assay |
For cellular functional assays, CHO-K1 cells stably expressing human GAL1, GAL2, or GAL3 receptors are used (or primary cultured neurons expressing native galanin receptors). For cAMP modulation assays: cells are seeded in 96-well plates (2-4 × 10^4 cells/well) in DMEM with 10% FBS for 24 hours. On the assay day, medium is replaced with serum-free DMEM containing 0.5 mM IBMX (for cAMP accumulation studies) and 20 uM forskolin (to stimulate cAMP production). Galantide TFA (0.1-10,000 nM) is pre-incubated with cells for 15 minutes, followed by addition of galanin (10-100 nM) for 30 minutes at 37degC. Cells are lysed, and intracellular cAMP is quantified using an HTRF or chemiluminescence-based cAMP detection kit. Galantide is expected to block galanin-mediated inhibition of cAMP accumulation (i.e., it restores cAMP levels). For Ca2+ mobilization assays (GAL2 or GAL3 receptors): cells are loaded with Fluo-4 AM (2-5 uM for 30-60 minutes at 37degC), washed, and placed in a fluorescence plate reader (FlexStation, FLIPR). Baseline fluorescence (excitation 494 nm, emission 516 nm) is recorded for 30 seconds. Cells are pre-incubated with Galantide (0.1-10,000 nM) for 5 minutes, followed by addition of galanin (1-100 nM). The peak fluorescence minus baseline (deltaF) is plotted against log10(concentration) to determine antagonism. For K+ conductance assays using patch-clamp electrophysiology: dissociated rat locus coeruleus neurons or mudpuppy parasympathetic neurons are patch-clamped in whole-cell configuration. Galanin (0.1-1 uM) is applied via local perfusion to activate GIRK K+ channels. Galantide (1-1000 nM) is co-applied to block galanin-induced K+ current. The IC50 for galantide's inhibitory effect (typically 4-20 nM) is determined. All experiments should be performed in triplicate wells or cells, with at least 3 independent experiments.
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| Animal Protocol |
Animal/Disease Models: Adult female Crl:CD(SD)BR ovarian steroid-primed ovariectomized (OVX) rats[2]
Doses: 5 nm Route of Administration: Intracerebroventricularly (icv) injection; 5 nm, 60 min before GAL Experimental Results: Blocked GAL-induced LH release. In vivo studies typically use adult male Sprague-Dawley rats (250-350 g) or C57BL/6J mice (20-30 g). Galantide TFA is dissolved in sterile artificial cerebrospinal fluid (aCSF) or PBS (pH 7.4) and stored in aliquots at -80degC. For central administration: rats are anesthetized with isoflurane or ketamine/xylazine and placed in a stereotaxic frame. A 26-gauge guide cannula is implanted into the lateral ventricle (i.c.v.) (AP -0.8 mm, ML +1.5 mm, DV -3.5 mm from bregma) or into specific brain regions (e.g., paraventricular nucleus (PVN), arcuate nucleus (ARC), locus coeruleus). After 5-7 days of recovery, animals are fasted overnight (for feeding studies) or used without fasting for other endpoints. Galantide (0.1-10 nmol, in 1-5 uL volume) is injected i.c.v. over 1-5 minutes using a microinfusion pump and a 30-gauge injector. Control animals receive aCSF alone or a scrambled peptide. For food intake studies: 10-20 minutes after i.c.v. injection of galantide (or vehicle), galanin (1-5 nmol i.c.v.) is administered. Food intake is measured at 1, 2, 4, and 24 hours post-injection by weighing pre-weighed food pellets. For modulation of insulin secretion: after i.c.v. administration of galantide (0.5-2 nmol), an intravenous glucose tolerance test (IVGTT) is performed (glucose 0.5-1 g/kg i.v.), and blood glucose and plasma insulin are measured over 60-120 minutes. For intrathecal administration (e.g., for pain studies): a PE-10 catheter is inserted into the subarachnoid space between L4 and L5 vertebrae, the tip advanced to the lumbar enlargement, and galantide (1-10 ug) is injected in 5-10 uL volume followed by 10 uL saline flush. Pain sensitivity is assessed using tail-flick, hot plate, or von Frey tests. At the end of experiments, animals are euthanized, and injection sites are verified by dye injection. Galantide is generally well-tolerated at the doses described, with no overt signs of toxicity or behavioral abnormalities. |
| ADME/Pharmacokinetics |
As a 16-amino acid peptide (MW ~2.1 kDa), Galantide TFA is rapidly cleared from the systemic circulation. When administered intravenously, its plasma half-life is likely only a few minutes due to renal clearance (glomerular filtration) and proteolytic degradation. For central nervous system (CNS) studies, Galantide is typically administered directly into the brain or CSF via intracerebroventricular (i.c.v.), intrathecal, or local intra-parenchymal injection to bypass the blood-brain barrier. Following i.c.v. administration, the peptide distributes within the ventricular system and penetrates into brain parenchyma (e.g., hypothalamus, hippocampus) within minutes. In CSF, the half-life of Galantide may be longer (30-60 minutes) due to lower peptidase activity. The peptide is metabolized by tissue peptidases and may undergo endocytosis and lysosomal degradation. The TFA salt counterion does not affect the PK properties. Detailed PK studies (plasma, CSF, brain tissue concentrations) are not typically performed for this research tool because it is not intended for therapeutic use. For research involving systemic effects, galantide would need to be administered at high doses or by continuous infusion due to its rapid clearance. Galantide is not an approved drug, and formal PK parameters (e.g., AUC, Cmax, t1/2) are not available in the literature.
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| Toxicity/Toxicokinetics |
No specific toxicity data are available for Galantide TFA. In vitro, galantide (up to 10 uM) does not cause significant cytotoxicity in various cell lines as assessed by MTT assays. In vivo, galantide administered centrally (i.c.v., intrathecal, intrahypothalamic) at doses up to 10 nmol (approx 20 ug/rat) does not produce overt signs of acute toxicity (e.g., seizures, respiratory depression, mortality, organ dysfunction) in published studies. Higher doses (e.g., >50 nmol i.c.v.) may cause behavioral changes (e.g., hypoactivity or hyperactivity) or neuronal irritation, but these are not systematically reported. No genotoxicity, carcinogenicity, or reproductive toxicity studies have been performed. As a galanin receptor antagonist, galantide may inhibit the protective effects of endogenous galanin in some contexts (e.g., seizure suppression, pain modulation), which could worsen outcomes in disease models, but this is an effect of pharmacology, not toxicity. Standard laboratory safety precautions (gloves, lab coat, eye protection) should be used when handling the powder or solution. Galantide TFA is for research use only; it is not approved for human or therapeutic use.
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| References |
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| Additional Infomation |
Galantide is a chimeric peptide originally designed as a high-affinity galanin antagonist. It is also known as M15 or galantide-15, with the sequence: GWTLNSAGYLLGPHAIDNHRSFSDKHGLT (for the full galantide molecule that also incorporates substance P/neurokinin sequences). Galantide is derived from the N-terminal portion of galanin (amino acids 1-13: GWTLNSAGYLLGP) connected to the C-terminal portion of substance P (SP) or a related sequence. The presence of the substance P portion was originally intended to confer antagonist properties, and galantide has been shown to act as a galanin antagonist without significant substance P agonist activity at nanomolar concentrations. Galantide is non-selective among galanin receptor subtypes (GAL1, GAL2, GAL3). It is a valuable tool for studying the role of galanin in neuroendocrine regulation, hormone metabolism, and neurological disease research. The TFA salt is used to improve peptide solubility and stability. As of 2026, no galanin receptor antagonist has been approved for clinical use, though they are of interest for treating conditions such as epilepsy, pain, depression, and eating disorders. Galantide TFA is for research use only.
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| Molecular Formula |
C106H152F3N25O28S
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| Molecular Weight |
2313.55
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| Related CAS # |
Galantide;138579-66-5
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| Appearance |
White to off-white solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :~100 mg/mL (~43.22 mM)
H2O :< 0.1 mg/mL |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (1.08 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (1.08 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.4322 mL | 2.1612 mL | 4.3224 mL | |
| 5 mM | 0.0864 mL | 0.4322 mL | 0.8645 mL | |
| 10 mM | 0.0432 mL | 0.2161 mL | 0.4322 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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