| Size | Price | Stock | Qty |
|---|---|---|---|
| 50mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| Other Sizes |
| ln Vitro |
Proglumide at concentrations between 0.3 and 10 mM decreased CCK-stimulated amylase release in an in vitro investigation; at concentrations between 0 and 3 mM, proglumide had no effect on baseline amylase release. The dose-response curve of CCK produced by amylase moves to the right as the concentration of proglumide rises. Proglumide's inhibitory action is reversible. Proglumide also has a selective impact on CCK and related peptides [2]. With an IC50 of 6.5 mM, proglumide treatment of HT29 cells dramatically decreased the incorporation of [3H]-thymidine into HT29 cells in a dose-dependent manner. Proglumide increases apoptosis by up to 70% while decreasing the percentage of necrosis in a dose-dependent manner [3].
|
|---|---|
| ln Vivo |
Proglumide (250-750 mg/kg; intraperitoneal injection; adult male Sprague-Dawley rats) is an effective treatment that greatly reduces brain oxidative stress, cognitive impairment, and seizure activity [1].
|
| Animal Protocol |
Animal/Disease Models: Induction of status epilepticus (SE) in adult male Sprague Dawley rats (200-250 g; 2 months old) [1]
Doses: 250 mg/kg, 500 mg/kg, and 750 mg/kg Route of Administration: Results of intraperitoneal (ip) injection: dose-dependent and significant increase in seizure and SE latency. Significant and dose-dependent attenuated Li-PC (SE)-induced increases in thiobarbituric acid (TBARS) and catalase (CAT), attenuated Li-Pc-induced decreases in SOD, and attenuated GSH and Depletion of glutathione-S transferase (GST). Hippocampus and striatum. SE Induction and Drug Treatment:** Adult male Sprague-Dawley rats were randomly assigned to groups. SE was induced by administering lithium chloride (3 mEq/mL/kg, i.p.) followed 20 hours later by pilocarpine (20 mg/mL/kg, s.c.). Proglumide, dissolved in saline, was administered intraperitoneally (i.p.) at doses of 250, 500, or 750 mg/kg, one hour before pilocarpine injection. Control groups received saline, lithium alone, pilocarpine alone, or Proglumide alone. After pilocarpine injection, animals were observed for behavioral alterations, including peripheral cholinergic signs, stereotyped movements, and seizure development. Latencies to first seizure and to SE were recorded, and 24-hour mortality was noted. [1] * **Morris Water Maze Test:** After SE induction and behavioral observation, a subset of animals (n=6-8 per group) was subjected to the Morris water maze test to assess cognitive function. The test was conducted over four consecutive days. Animals were trained to find a hidden platform in a pool of water. The latency to reach the platform was recorded for each trial. Proglumide-pretreated groups were compared to control and SE groups. [1] * **Biochemical Analysis for Oxidative Stress:** One hour after lithium-pilocarpine treatment, the remaining animals were euthanized by decapitation. Brains were removed, and the hippocampus and striatum were dissected on ice. Tissues were homogenized and used for the determination of oxidative stress indices: TBARS (lipid peroxidation), reduced glutathione (GSH), glutathione-S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD) using established spectrophotometric methods. [1] |
| References |
|
| Additional Infomation |
Proglutamine is a racemic mixture composed of equal amounts of (R)-proglutamine and (S)-proglutamine. It is a non-selective cholecystokinin (CCK) antagonist, formerly used primarily for the treatment of gastric ulcers, but has been superseded by newer drugs. Proglutamine has multiple functions, including as a drug metabolite, xenobiotic metabolite, cholinergic antagonist, anti-ulcer drug, cholecystokinin antagonist, gastrointestinal drug, delta-opioid receptor agonist, and opioid analgesic. It contains (R)-proglutamine and (S)-proglutamine. Proglutamine is an orally bioavailable cholecystokinin (CCK) receptor antagonist with acid-reducing and potential antitumor activity. After oral administration, proglutamine binds to and blocks the activity of cholecystokinin receptor type A (CCK-AR; CCK1-R) and gastrin/cholecystokinin receptor type B (CCK-BR; CCK2-R). This prevents cholecystokinin and gastrin from binding to CCK receptors, thereby inhibiting gastrointestinal motility and gastric juice secretion. Furthermore, proglutamine may reduce fibrosis in the tumor microenvironment (TME), increase T-cell infiltration and chemotherapeutic drug penetration, and inhibit tumor growth and metastasis. CCK receptors are normally expressed in the gastrointestinal tract and nervous system, but are overexpressed in fibroblasts and some cancer cells. Proglutamine is a drug that inhibits gastric juice secretion and reduces gastrointestinal motility, and is clinically used to treat gastrointestinal ulcers.
|
| Exact Mass |
334.189
|
|---|---|
| CAS # |
6620-60-6
|
| Related CAS # |
Proglumide sodium;99247-33-3;Proglumide hemicalcium;85068-56-0
|
| PubChem CID |
4922
|
| Appearance |
White to off-white solid powder
|
| Density |
1.1±0.1 g/cm3
|
| Boiling Point |
589.8±45.0 °C at 760 mmHg
|
| Melting Point |
148.5--152ºC
|
| Flash Point |
310.5±28.7 °C
|
| Vapour Pressure |
0.0±1.7 mmHg at 25°C
|
| Index of Refraction |
1.534
|
| LogP |
2.53
|
| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
10
|
| Heavy Atom Count |
24
|
| Complexity |
413
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
O=C(O)CCC(NC(C1=CC=CC=C1)=O)C(N(CCC)CCC)=O
|
| InChi Key |
DGMKFQYCZXERLX-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C18H26N2O4/c1-3-12-20(13-4-2)18(24)15(10-11-16(21)22)19-17(23)14-8-6-5-7-9-14/h5-9,15H,3-4,10-13H2,1-2H3,(H,19,23)(H,21,22)
|
| Chemical Name |
4-benzamido-5-(dipropylamino)-5-oxopentanoic acid
|
| Synonyms |
Proglumide W-5219 W 5219W5219
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ≥ 65 mg/mL (~194.37 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.17 mg/mL (6.49 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 21.7 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: ≥ 2.17 mg/mL (6.49 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 21.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.17 mg/mL (6.49 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT04814602 | COMPLETED | Drug: Proglumide | Cirrhosis, Liver | Georgetown University | 2021-03-30 | Early Phase 1 |
| NCT04152473 | COMPLETED | Drug: Proglumide | Nonalcoholic Steatohepatitis | Georgetown University | 2019-12-13 | Phase 1 |
| NCT05551858 | ACTIVE, NOT RECRUITING | Drug: Proglumide Drug: Placebo |
Pain Pancreas Fibrosis Safety Issues |
Georgetown University | 2022-11-17 | Phase 1 Phase 2 |
| NCT05827055 | RECRUITING | Drug: Gemcitabine Drug: Nab paclitaxel Drug: Proglumide Drug: Placebo |
Metastatic Pancreatic Cancer | Georgetown University | 2024-01-31 | Phase 2 |
| NCT06017323 | WITHDRAWN | Drug: Gemcitabine Drug: Nab paclitaxel Drug: Proglumide Dose level 1 Drug: Proglumide Dose level 2 |
Metastatic Pancreatic Cancer | Georgetown University | 2023-10 | Phase 1 |
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
