2. Membrane Transporter/Ion Channel Neuronal Signaling
  3. TRP Channel
  4. DD-161515

DD-161515 is a TRPV1/VR1 inhibitor with an IC50 of 0.7 μM in rats. DD-161515 binds to an allosteric site of TRPV1 distinct from that of capsaicin, blocks channel opening, inhibits receptor-mediated calcium ion influx, reduces the excitability of peripheral sensory nerve fibers, and thereby inhibits nociception induced by heat and transmission of chemically induced pain signals. DD-161515 can be used in studies related to inflammatory pain.

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DD-161515

DD-161515 Chemical Structure

CAS No. : 410080-55-6

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DD-161515 Related Antibodies

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Description

DD-161515 is a TRPV1/VR1 inhibitor with an IC50 of 0.7 μM in rats. DD-161515 binds to an allosteric site of TRPV1 distinct from that of capsaicin, blocks channel opening, inhibits receptor-mediated calcium ion influx, reduces the excitability of peripheral sensory nerve fibers, and thereby inhibits nociception induced by heat and transmission of chemically induced pain signals. DD-161515 can be used in studies related to inflammatory pain[1][2].

IC50 & Target[2]

rTRPV1

0.7 μM (IC50)

In Vitro

DD-161515 preferentially inhibits TRPV1 channel activity with micromolar potency and moderate voltage-dependency[1].
DD-161515 acts as a potent, noncompetitive antagonist of recombinant rat VR1 channels expressed in Xenopus oocytes, with an IC50 of 0.7 μM[2].
DD-161515 inhibits capsaicin-evoked Ca2+ influx in ~70% of cultured newborn mouse trigeminal primary sensory neurons by ≥ 90% at 100 μM, with reversible blockade[2].

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

DD-161515 Related Antibodies
In Vivo

DD-161515 (0.2 mmol/kg; i.p.; single administration) transiently alleviates heat nociception at 52°C, significantly prolongs the response latency in the hot-plate test compared with the vehicle group; increases the tail-flick latency by 40% relative to the vehicle control group, exhibiting heat analgesic activity; and significantly alleviates mustard oil-induced heat hyperalgesia[2].
DD-161515 (0.05-0.2 mmol/kg; i.p.; single administration) dose-dependently abolishes capsaicin-induced pain behaviors and prevents neurogenic inflammation[2].
DD-161515 (0.4 μmol; intra-arterial administration; single dose) reversibly inhibits capsaicin-induced activation of knee joint nociceptor fibers[2].

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

Animal Model: ICR (adult male)[2]
Dosage: 0.05 mmol/kg; 0.1 mmol/kg; 0.2 mmol/kg
Administration: i.p.; single dose
Result: Increased latency to first pain behavior 13-fold to 269 s at 0.2 mmol/kg compared to vehicle latency of 20 s, and reduced pain behavior duration to near zero.
Increased latency to first pain behavior to 80 s at 0.05 mmol/kg.
Prevented capsaicin-induced ipsilateral paw volume increase at 0.05 mmol/kg and 0.2 mmol/kg, with ipsilateral paw volumes measuring 15.3 mm3 and 15.2 mm3 respectively, compared to vehicle-treated mice where ipsilateral paw volume was 20.6 mm3.
Molecular Weight

645.45

Formula

C29H37Cl4N5O3
CAS No.
SMILES

O=C(CN(CCC1=CC=C(C=C1Cl)Cl)C(CN(CCC2=CC=C(C=C2Cl)Cl)C(CNCCC3N(CCC3)C)=O)=O)N
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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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DD-161515 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:

DD-161515410080-55-6DD161515DD 161515TRP ChannelTransient receptor potential channelsTRPV1neurogenic inflammationthermal hyperalgesiainflammatory painthermal nociceptionratXenopus oocytesVR1calcium influxmouse trigeminal primary sensory neuronsInhibitorinhibitorinhibit

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