2. Stem Cell/Wnt TGF-beta/Smad Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Apoptosis
  3. PKA Reactive Oxygen Species (ROS) Apoptosis
  4. Bucladesine

Bucladesine (Dibutyryl cAMP; DBcAMP) is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependent protein kinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation.

For research use only. We do not sell to patients.

CAS No. : 362-74-3

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Bucladesine Related Antibodies

Top Publications Citing Use of Products

41 Publications Citing Use of MCE Bucladesine

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Cell Proliferation/Viability Assay

    Bucladesine purchased from MedChemExpress. Usage Cited in: Int J Biol Sci. 2024 Aug 19;20(11):4476-4495.  [Abstract]

    The protein expression of p-AMPK (S173), p-AMPK (T172) and AMPK of HT-29 cells treated with 5-HT, either alone or in combination with H-89 (1 μM) and dbcAMP (1 μM).

    Bucladesine purchased from MedChemExpress. Usage Cited in: Ecotoxicol Environ Saf. 2022 Sep 15:243:113982.  [Abstract]

    H295R cells were treated with 30 μM BHPF in the absence or presence of 10 μM forskolin (FSK) or 100 μM dbcAMP for 48 h and evaluated by Western blotting.

    Bucladesine purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2022 Oct 15:932:175231.  [Abstract]

    B16F10 cells was pretreated or not with 3 μM Bucladesine sodium for 1 h before pterostilbene was applied for 24 h, 48h or 72 h at 3 μM. The CREB and p-CREB protein expression levels were detected by WB.

    Bucladesine purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2022 Oct 15:932:175231.  [Abstract]

    Cell viability of H295R cells exposed to 0–40 μM BHPF in the presence of 100 μM dbcAMP for 48 h.

    Bucladesine purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2022 Oct 15:932:175231.  [Abstract]

    Micrographs presenting the incorporation of EdU in H295R cells exposed to BHPF or combined with 100 μM dbcAMP for 48 h. Red: the EdU positive cells; blue: the cell nuclei (Hoechst).

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    Description

    Bucladesine (Dibutyryl cAMP; DBcAMP) is a membrane-permeable 3′, 5′-cyclic adenosine monophosphate (cAMP) analog. Bucladesine selectively activates cAMP dependent protein kinase (PKA) by increasing the intracellular level of cAMP. Bucladesine significantly attenuates MDMA-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio, thereby improving spatial learning and memory impairments. Bucladesine exhibit anti-nociceptive and anti-inflammation effect. Bucladesine can inhibit cancer cells proliferation, induce apoptosis. Bucladesine can be used for the researches of neurological disease, cancer, inflammation[1][2][3][4].

    Cellular Effect
    Cell Line Type Value Description References
    RAW264.7 IC50
    28.9 μM
    Compound: dbcAMP
    Antiinflammatory activity against mouse RAW264.7 cells assessed as inhibition of LPS-induced TNFalpha production after 4 hrs by ELISA
    Antiinflammatory activity against mouse RAW264.7 cells assessed as inhibition of LPS-induced TNFalpha production after 4 hrs by ELISA
    		[PMID: 11000020]
    In Vitro

    Bucladesine causes significant growth delay in multicellular tumor spheroids derived directly from human malignant brain tumors[1].
    Bucladesine augments differentiation therapy (in combination with Sodium butyrate (HY-B0350A) and hyperthermia) in human and canine brain tumor cells in vitro[1].
    Bucladesine suppresses the mitogenic effects of platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), and epidermal growth factor (EGF) on human astrocytoma cells; bucladesine alone neither potentiates nor inhibits human astrocytoma cell growth[1].
    Bucladesine suppresses proliferation, enhances cytoplasmic process formation, increases cytoplasmic glial fibrillary acidic protein (GFAP) levels, and suppresses malignant glioma invasion by decreasing CD44 isoform expression in cultured malignant glioma cells, inducing biochemical and morphological changes[1].
    Bucladesine decreases Bcl-2 levels and enhances SNAP-induced p53-sensitive cell death and MPP+-induced cell death, sensitizing human neuroblastoma cells to apoptosis[1].
    Bucladesine inhibits proliferation and induces morphological differentiation of astrocytes in vitro via a cyclic adenosine monophosphate-dependent protein kinase pathway[1].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Bucladesine Related Antibodies
    In Vivo

    Bucladesine (100 μM; bilateral intrahippocampal infusion; once daily; 4 consecutive days) significantly attenuates 3,4-methylenedioxymethamphetamine (MDMA)-induced spatial learning and memory impairments and hippocampal mitochondrial dysfunction in adult male Wistar rats[2].
    Bucladesine (50-300 nM/mouse; i.p.; single dose) exerts a biphasic anti-nociceptive effect on thermal-induced acute pain in male albino mice, with significant activity at 50 and 100 nM/mouse doses, no significant effect at 300 nM/mouse[3].
    Bucladesine (0.5-1.5% cream, 5% solution; topical; single or two doses) produces a statistically significant reduction in Arachidonic acid (HY-109590)-induced acute skin inflammation in Mus musculus, with single administration of 1.5% cream yielding a 28% reduction in ear swelling and two administrations yielding a 24% reduction[4].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: Wistar rats (adult male, 3-4 months old, 200-250 g, intrahippocampal infusion of 0.5 or 1 μg/side MDMA)[2]
    Dosage: 10 μM; 100 μM
    Administration: bilateral intrahippocampal infusion; once daily; 4 consecutive days
    Result: Significantly reduced MDMA (0.5 and 1 μg/side)-induced increases in mean escape latency and traveled distance across 4 MWM training days.
    Significantly increased MDMA (0.5 and 1 μg/side)-reduced time spent in the target quadrant, traveled distance in the target quadrant, and number of platform site crossings during the MWM probe test.
    Significantly attenuated MDMA (0.5 and 1 μg/side)-induced increases in hippocampal mitochondrial ROS formation, mitochondrial outer membrane damage, cytochrome c release, and hippocampal ADP/ATP ratio.
    Significantly reduced MDMA (0.5 and 1 μg/side)-induced mitochondrial membrane potential collapse and mitochondrial swelling.
    Did not produce a significant reduction in MDMA-induced spatial learning and memory dysfunction at 10 μM, so mitochondrial function was not assessed for this dose.
    Animal Model: albino mice (male, 25-30 g)[3]
    Dosage: 50 nM/mouse; 100 nM/mouse; 300 nM/mouse
    Administration: i.p.; single dose 15 minutes pre-test
    Result: Significantly increased tail-flick latency relative to control at 50 nM/mouse and 100 nM/mouse doses.
    Did not significantly alter tail-flick latency relative to control at 300 nM/mouse dose.
    Enhanced the anti-nociceptive effect of pentoxifylline when co-administered with 5 mg/100g Pentoxifylline (HY-B0715) at 300 nM/mouse dose.
    Animal Model: Arachidonic acid-induced acute skin inflammation Mus musculus (male, 20-30 g)[4]
    Dosage: 0.5% (cream); 1.5% (cream); 5% (solution)
    Administration: topical; single dose (3 hours pre-challenge for cream, 60 minutes pre-challenge for solution); two doses (7 hours and 3 hours pre-challenge for cream)
    Result: Reduced arachidonic acid-induced ear swelling by 10% (0.5% cream, single administration).
    Reduced arachidonic acid-induced ear swelling by 28% (1.5% cream, single administration).
    Reduced arachidonic acid-induced ear swelling by 10% (0.5% cream, two administrations).
    Reduced arachidonic acid-induced ear swelling by 24% (1.5% cream, two administrations).
    Reduced arachidonic acid-induced ear swelling by 18% (5% solution, single administration).
    Molecular Weight

    469.39

    Formula

    C18H24N5O8P
    CAS No.
    SMILES

    O=C(CCC)O[C@H]1[C@H](N2C(N=CN=C3NC(CCC)=O)=C3N=C2)O[C@@](CO4)([H])[C@@]1([H])OP4(O)=O
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.
    Purity & Documentation
    References
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    Bucladesine Related Classifications

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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    Bucladesine362-74-3Dibutyryl cAMP DBcAMPPKAReactive Oxygen Species (ROS)ApoptosisProtein kinase AEGFmalignant gliomaBcl-2hippocampalMPP+bFGFastrocytep53PDGFInhibitorinhibitorinhibit

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