Cat. No.: HY-19876

PL37

Name: PL37
Brand: MedChemExpress
SKU: HY-19876
Availability: PreOrder

(Synonyms: Debio-0827)

PL37 (Debio-0827) is an orally active, blood-brain barrier permeable dual enkephalinase inhibitor. PL37 inhibits aminopeptidase N, neprilysin, and metalloproteases, thereby blocking the degradation of endogenous enkephalins, elevating enkephalin levels, and activating peripheral μ- and δ-opioid receptors. PL37 induces mitochondrial dysfunction, mitophagy, and apoptosis, inhibits endothelial cell proliferation, migration, invasion, and tube formation, and suppresses hemangioma tumor growth and angiogenesis. PL37 can be used in research related to peripheral neuropathic pain, osteosarcoma-induced hyperalgesia, painful diabetic neuropathy, migraine, bone cancer pain, neuroinflammatory pain, and infantile hemangioma.

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

CAS No.: 935481-06-4
Formula: C₂₂H₃₄N₂O₆S₃
Molecular Weight:518.71

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (300 KB)

PL37 Chemical Structure

CAS No.: 935481-06-4

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Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]

aminopeptidase N

δ Opioid Receptor/DOR

μ Opioid Receptor/MOR

enkephalinase

All Opioid Receptor Isoforms :

All Aminopeptidase Isoforms :

CD13
LTA4H

All MMP Isoforms :

In Vitro

PL37 (Debio-0827) (100.6-116.7 μM; 24-96 h) potently inhibits the proliferation of HUVECs (IC₅₀ = 100.6 μM) and HemECs (IC₅₀ = 116.7 μM) in dose- and time-dependent manners^[9].
PL37 (70 μM; 12-24 h) potently inhibits the migration of HUVECs and HemECs, resulting in <10% wound closure in HUVECs at 24 h^[9].
PL37 (100 μM; 24 h) potently inhibits the invasive ability of HUVECs and HemECs, reducing the number of cells that penetrate the Matrigel membrane^[9].
PL37 (100 μM; 24 h) potently induces apoptosis in HUVECs and HemECs^[9].
PL37 (100 μM; 3-9 h) potently disrupts tubular network assembly in HUVECs and HemECs, inhibiting both branch point formation and capillary length in HUVECs and branch point formation in HemECs^[9].
PL37 (100 μM; 24 h) induces marked mitochondrial fragmentation and structural disorganization in HUVECs and HemECs, significantly reducing mitochondrial aspect ratios compared to control and Propranolol (HY-B0573B)-treated cells^[9].
PL37 (100 μM; 24 h) potently induces mitochondrial membrane potential collapse in HUVECs and HemECs, resulting in a significantly lower red/green fluorescence ratio than control and propranolol-treated cells^[9].
PL37 (100 μM; 24 h) potently induces excessive mitochondrial ROS production in HUVECs and HemECs^[9].
PL37 (100 μM; 24 h) induces severe mitochondrial ultrastructural damage and activates mitophagy in HUVECs and HemECs, as evidenced by swollen mitochondria, disorganized cristae, and increased mitophagosomes^[9].

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

Cell Cytotoxicity Assay^[9]

Cell Line:

human umbilical vein endothelial cells (HUVECs), hemangioma-derived endothelial cells (HemECs)
Concentration:

100.6 μM (HUVEC IC₅₀); 116.7 μM (HemEC IC₅₀)
Incubation Time:

24 h (dose-response); 24-96 h (time-dependent analysis)
Result:

Potently inhibited proliferation of both cell lines, with an IC₅₀ of 100.6 μM in HUVECs and 116.7 μM in HemECs.
Suppressed cell viability in a time-dependent manner over 24 to 96 h at IC₅₀ concentrations, with viability dropping to ~25% in HUVECs and ~10% in HemECs by 96 h.

Apoptosis Analysis^[9]

Cell Line:

human umbilical vein endothelial cells (HUVECs), hemangioma-derived endothelial cells (HemECs)
Concentration:

100 μM
Incubation Time:

24 h
Result:

Markedly induced apoptosis in both cell lines, increasing the apoptotic rate by approximately 2-fold in HUVECs and 15-fold in HemECs compared with control groups.
Increased apoptotic rate to ~50% in HUVECs and ~32% in HemECs.

Cell Migration Assay ^[9]

Cell Line:

human umbilical vein endothelial cells (HUVECs), hemangioma-derived endothelial cells (HemECs)
Concentration:

70 μM
Incubation Time:

12-24 h post-wounding
Result:

Markedly suppressed cell motility, with HUVECs exhibiting <10% wound closure at 24 h, compared to 50% in control and 30% in propranolol-treated groups.
Exerted corresponding inhibitory effect in HemECs.

Cell Invasion Assay^[9]

Cell Line:

human umbilical vein endothelial cells (HUVECs), hemangioma-derived endothelial cells (HemECs)
Concentration:

100 μM
Incubation Time:

24 h post-attachment
Result:

Significantly reduced the number of cells penetrating the Matrigel membrane in both cell lines.

Immunofluorescence^[9]

Cell Line:

human umbilical vein endothelial cells (HUVECs), hemangioma-derived endothelial cells (HemECs)
Concentration:

100 μM
Incubation Time:

24 h
Result:

Induced more pronounced mitochondrial fragmentation and structural disorganization than propranolol.
Significantly reduced the aspect ratio of mitochondria in both HUVECs and HemECs.

In Vivo

PL37 (Debio-0827) (70 mg/kg; i.p.; single dose) produces a short-lived (maximal at 20 minutes) significant antiallodynic effect against mechanical static allodynia in Vincristine (HY-N0488A)-induced neuropathic rats, with no activity on cold allodynia^[1].
PL37 (50-100 mg/kg; p.o.; single dose) produces short-lived (maximal at 20 minutes), dose-dependent antiallodynic and anti-hypersensitive effects against mechanical static allodynia, mechanical dynamic allodynia, and mechanical dynamic hypersensitivity in vincristine-induced neuropathic rats, with no activity on cold allodynia^[1].
PL37 (100 mg/kg; p.o.; single dose) has short-lived antiallodynic and anti-hypersensitive effects against mechanical static allodynia and mechanical dynamic hypersensitivity in vincristine-induced neuropathic rats that are fully reversed by peripheral opioid receptor antagonist Naloxone-methiodide (HY-137279), confirming a peripheral opioid-mediated mechanism^[1].
PL37 (50-100 mg/kg; p.o.; single dose) completely inhibits acute Isosorbide Dinitrate (HY-B1409)-induced cephalic mechanical hypersensitivity in male Sprague-Dawley rats, with median von Frey withdrawal thresholds of 6.0 g and 8.0 g, respectively, at 1 hour post-treatment^[4].
PL37 (20 mg/kg; i.v.; single dose) inhibits chronic isosorbide dinitrate-induced cephalic mechanical hypersensitivity in male Sprague-Dawley rats, with a median von Frey withdrawal threshold of 4.0 g at 1 hour post-treatment, while single oral doses of 50-100 mg/kg show no effect^[4].
PL37 (50-100 mg/kg; p.o.; daily; 5 days) prevents chronic and interictal isosorbide dinitrate-induced cephalic mechanical hypersensitivity in male Sprague-Dawley rats, and 100 mg/kg daily treatment reduces touch-evoked trigeminocervical complex c-Fos expression by 54.1% in laminae I-IIo^[4].
PL37 (100 mg/kg; p.o.; single dose; daily; 5 days; 20 mg/kg; i.v.; single dose) has no effect on cephalic mechanical sensitivity in naive male Sprague-Dawley rats^[4].
PL37 (0.25-6.25 mg/kg; p.o.; single dose) dose-dependently inhibits ISDN-induced cephalic mechanical hypersensitivity in male Sprague-Dawley rats with an ED₅₀ of 1.1 mg/kg^[5].
PL37 (68.75-275 μg; p.o.; single dose, in fixed-ratio combinations with Sumatriptan (HY-B0121B)) acts synergistically with sumatriptan to inhibit ISDN-induced cephalic mechanical hypersensitivity in male Sprague-Dawley rats, with an interaction index of 0.14^[5].
PL37 (Debio-0827) (2.1-25 mg/kg; p.o.; single dose) dose-dependently inhibits osteosarcoma-induced thermal hyperalgesia in male C3H/HeJ mice, with an ED₅₀ of 16.52 mg/kg, and produces synergistic antihyperalgesic effects when combined with A-317491 (HY-15568)^[8].
PL37 (10-20 mg/kg; i.v., p.o.; single dose; 1 hour before behavioral testing or SNP injection) significantly attenuates stress-induced migraine-like behaviors and SNP-primed hypersensitivity in mice via activation of peripheral delta-opioid receptors^[10].
PL37 (12.5-50 mg/kg; p.o.; single dose) dose-dependently inhibits osteosarcoma-induced thermal hyperalgesia in C3H/HeJ mice, with 25 mg/kg PL37 producing complete peripheral antihyperalgesia mediated exclusively by μ-opioid receptors, and subeffective PL37 synergistically interacts with subeffective Gabapentin (HY-A0057) to completely suppress thermal hyperalgesia^[2].
PL37 (20 mg/kg; i.t.; daily; 10 days) exhibits potent anti-hemangioma activity in BALB/C-nude mice, reducing tumor volume by 79.94% and tumor weight by 83% via inhibition of angiogenesis and activation of mitochondrial-mediated apoptosis, without observable toxicity^[9].

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

Animal Model:

Sprague-Dawley (adult male, 312.3 g weight at study start, vincristine-induced peripheral neuropathic pain model)^[1]
Dosage:

70 mg/kg
Administration:

i.p.; single dose
Result:

Increased the Δ-paw withdrawal threshold by 8.14 arbitrary units at 20 minutes post-administration.
Showed no significant effect on Δ-paw withdrawal threshold at 50 minutes post-administration.
Had no effect on cold allodynia scores.

Animal Model:

Sprague-Dawley (adult male, 312.3 g weight at study start, vincristine-induced peripheral neuropathic pain model)^[1]
Dosage:

50 mg/kg; 100 mg/kg
Administration:

p.o.; single dose
Result:

Increased the Δ-paw withdrawal threshold by 3.4 arbitrary units at 20 minutes post-administration with 50 mg/kg, and by 14.36 arbitrary units at 20 minutes post-administration with 100 mg/kg.
Produced a 75% decrease in positive responses in smooth paint-brush test at 20 minutes post-administration with 100 mg/kg, while 50 mg/kg showed a non-significant reduction.
Produced a 37.9% decrease in positive responses in rough paint-brush test at 20 minutes post-administration with 50 mg/kg, and a 75.86% decrease with 100 mg/kg.
Had no effect on cold allodynia scores.
All significant effects returned to baseline at 50 minutes post-administration.

Animal Model:

Sprague-Dawley (adult male, 312.3 g weight at study start, vincristine-induced peripheral neuropathic pain model)^[1]
Dosage:

100 mg/kg
Administration:

p.o.; single dose
Result:

Significantly increased the Δ-paw withdrawal threshold at 20 minutes post-administration when administered alone, but this effect was completely antagonized by co-administration with naloxone-methiodide.
Significantly decreased positive responses in rough paint-brush test at 20 minutes post-administration when administered alone, but this effect was completely antagonized by co-administration with naloxone-methiodide.
Effects returned to baseline at 50 minutes post-administration.

Animal Model:

C3H/HeJ (5-6 week old, 26-33 g, male/female, intratibially inoculated with NCTC 2472 osteosarcoma cells)^[2]
Dosage:

12.5 mg/kg; 25 mg/kg; 50 mg/kg; 13.4 mg/kg (ED₅₀, PL37 alone); 7.03 mg/kg (ED₅₀, combination with gabapentin)
Administration:

p.o.; single dose
Result:

Completely suppressed osteosarcoma-induced thermal hyperalgesia at 25 mg/kg, with peak effect at 20-40 minutes post-administration and effect resolving by 60 minutes, restricted to the tumor-inoculated paw.
Prolonged withdrawal latencies in both the tumor-inoculated and contralateral paws at 50 mg/kg.
Exhibited no standalone antihyperalgesic effect at 12.5 mg/kg.
Had an ED₅₀ of 13.4 mg/kg when administered alone.
Showed synergistic interaction with subeffective gabapentin (6.25 mg/kg, i.p.) at subeffective dose of 12.5 mg/kg, completely inhibiting osteosarcoma-induced thermal hyperalgesia.
Had an experimental ED₅₀ of 7.03 mg/kg in combination with gabapentin, significantly lower than the theoretical additive ED₅₀ of 12.8 mg/kg, with an interaction index of 0.55.
Had antihyperalgesic effect at 25 mg/kg completely blocked by peripheral opioid antagonist naloxone-methiodide (2 mg/kg, i.p.) and selective μ-opioid receptor antagonist cyprodime (1 mg/kg, s.c.), but not by δ-opioid receptor antagonist naltrindole (0.1 mg/kg, s.c.) or κ-opioid receptor antagonist nor-binaltorphimine (10 mg/kg, s.c.).
Had bilateral analgesic effect at 50 mg/kg only partially reduced by naloxone-methiodide.

Animal Model:

Sprague-Dawley (male, 250-275 g, isosorbide dinitrate-induced acute cephalic mechanical hypersensitivity)^[4]
Dosage:

50 mg/kg; 100 mg/kg
Administration:

p.o.; single dose
Result:

Completely inhibited isosorbide dinitrate-induced acute cephalic mechanical hypersensitivity.
Reached median von Frey withdrawal thresholds of 6.0 g at 1 hour post-administration for 50 mg/kg dose.
Reached median von Frey withdrawal thresholds of 8.0 g at 1 hour post-administration for 100 mg/kg dose.

Animal Model:

Sprague-Dawley (male, 250-275 g, isosorbide dinitrate-induced chronic cephalic mechanical hypersensitivity)^[4]
Dosage:

50 mg/kg (oral, no effect); 100 mg/kg (oral, no effect); 20 mg/kg (i.v., active)
Administration:

p.o.; single dose; i.v.; single dose
Result:

Failed to inhibit chronic cephalic mechanical hypersensitivity at oral doses of 50 mg/kg and 100 mg/kg.
Significantly decreased chronic cephalic mechanical hypersensitivity at i.v. dose of 20 mg/kg.
Reached median von Frey withdrawal threshold of 4.0 g at 1 hour post-administration for 20 mg/kg i.v. dose.

Animal Model:

Sprague-Dawley (male, 250-275 g, isosorbide dinitrate-induced chronic and interictal cephalic mechanical hypersensitivity)^[4]
Dosage:

50 mg/kg; 100 mg/kg
Administration:

p.o.; daily; 5 days
Result:

Reduced chronic cephalic mechanical hypersensitivity after the 5th isosorbide dinitrate injection, with median von Frey withdrawal thresholds of 3.0 g for 50 mg/kg dose and 4.0 g for 100 mg/kg dose at 1 hour post-administration.
Suppressed persistent interictal cephalic mechanical hypersensitivity induced by 4 consecutive isosorbide dinitrate injections.
Decreased touch-evoked c-Fos expression in the ipsilateral trigeminocervical complex by 54.1% within laminae I-IIo at 100 mg/kg dose.

Animal Model:

Sprague-Dawley (male, 250-275 g, naive)^[4]
Dosage:

100 mg/kg (p.o. single); 20 mg/kg (i.v. single); 100 mg/kg (p.o. daily)
Administration:

p.o.; single dose; i.v.; single dose; p.o.; daily; 5 days
Result:

Showed no effect on cephalic mechanical sensitivity at single oral 100 mg/kg dose.
Showed no effect on cephalic mechanical sensitivity at single i.v. 20 mg/kg dose.
Showed no effect on cephalic mechanical sensitivity at repeated daily oral 100 mg/kg dose for 5 days.

Animal Model:

Sprague-Dawley (male, 235-275 g, migraine model induced by intraperitoneal isosorbide dinitrate injection)^[5]
Dosage:

0.25 mg/kg; 1.0 mg/kg; 1.5 mg/kg; 2.0 mg/kg; 6.25 mg/kg
Administration:

p.o.; single dose
Result:

Produced a dose-dependent inhibition of ISDN-induced cephalic mechanical hypersensitivity.
Showed no significant effect at 0.25 mg/kg and 1.0 mg/kg doses.
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 76.3% at 1.5 mg/kg (p=0.003).
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 69.3% at 2.0 mg/kg (p=0.002).
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 75.1% at 6.25 mg/kg (p<0.001).
Achieved a median effective dose (ED₅₀) of 1.1 mg/kg.

Animal Model:

Sprague-Dawley (male, 235-275 g, migraine model induced by intraperitoneal isosorbide dinitrate injection)^[5]
Dosage:

68.75 μg (in combination with 18.75 μg sumatriptan; ED₅₀/16 ratio); 137.5 μg (in combination with 37.5 μg sumatriptan; ED₅₀/8 ratio); 275 μg (in combination with 75 μg sumatriptan; ED₅₀/4 ratio)
Administration:

p.o.; single dose
Result:

Produced a dose-dependent inhibition of ISDN-induced cephalic mechanical hypersensitivity when administered in fixed-ratio combinations with sumatriptan.
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 35.5% at the ED₅₀/16 ratio (p=0.039).
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 77.4% at the ED₅₀/8 ratio (p<0.004).
Reduced the area over the curve (AOC) of cephalic hypersensitivity by 98.4% at the ED₅₀/4 ratio (p<0.001).
Achieved an experimental ED₅₀ of 0.10 mg/kg for the combination, which was significantly lower than the theoretical additive ED₅₀ of 0.71 mg/kg.
Resulted in an interaction index of 0.14.
Confirmed significant synergistic effects via isobolographic analysis.

Animal Model:

C3H/HeJ (5- to 6-week-old male; bone cancer pain model via intratibial inoculation of NCTC 2472 fibrosarcoma cells)^[8]
Dosage:

2.1 mg/kg (1/8 of ED₅₀); 2.36 mg/kg (1/7 of ED₅₀); 2.75 mg/kg (1/6 of ED₅₀); 4.13 mg/kg (1/4 of ED₅₀); 12.5 mg/kg; 18.7 mg/kg; 25 mg/kg; 2.51 mg/kg (combination ED₅₀)
Administration:

p.o.; single dose
Result:

Completely inhibited osteosarcoma-induced thermal hyperalgesia at 25 mg/kg.
Dose-dependently attenuated thermal hyperalgesia at 12.5, 18.7, and 25 mg/kg.
Achieved an ED₅₀ of 16.52 mg/kg for oral administration.
Produced synergistic antihyperalgesic effects when coadministered with fixed ratios of A-317491, with an experimental combination ED₅₀ of 2.51 mg/kg (significantly lower than the theoretical additive ED₅₀ of 8.32 mg/kg) and an interaction index of 0.284.
Achieved complete antihyperalgesia with the 1/6 ED₅₀ ratio combination.

Animal Model:

BALB/C-nude (female, 6 weeks old, ~20 g, subcutaneous injection of 2.5 × 10⁶ HemEC cells suspended in 100 μL Matrigel into dorsal region)^[9]
Dosage:

20 mg/kg
Administration:

i.t.; daily; 10 days
Result:

Reduced tumor volume by 79.94%.
Reduced tumor weight by 83%.
Suppressed microvessel formation.
Markedly suppressed VEGF and MMP9 expression.
Elevated levels of Caspase-3 and cytochrome c.
Caused no significant changes in organ structure or mouse body weight.

Animal Model:

ICR mice (6- to 8-week-old, male and female, 25 to 34 g; repetitive restraint stress-induced migraine model)^[10]
Dosage:

10 mg/kg (i.v.); 20 mg/kg (p.o.)
Administration:

i.v.; single dose; 1 hour before behavioral testing or SNP injection; p.o.; single dose; 1 hour before behavioral testing or SNP injection
Result:

Significantly increased periorbital withdrawal thresholds and reduced facial grimace scores in male and female mice compared to vehicle on day 2 post-stress.
Significantly increased periorbital withdrawal thresholds at 1 and 3 hours post-administration in males and females, and at 5 hours post-administration in males only; reduced grimace scores at 1, 3, and 5 hours post-administration in both sexes (10 mg/kg i.v.).
Significantly increased facial withdrawal thresholds at 1 and 3 hours after SNP injection in male and female mice on day 14 post-stress.
Had effects blocked by delta-opioid receptor antagonist naltrindole (0.1 mg/kg) and peripherally restricted opioid receptor antagonist naloxone methiodide (5 mg/kg), but not by mu-opioid receptor antagonist CTAP (1 mg/kg).

Chemical Information

CAS No. 935481-06-4
Molecular Weight 518.71
Formula C₂₂H₃₄N₂O₆S₃
SMILES

CSCC[C@H](N)CSSC[C@@H](CC1=CC=CC=C1)C(NCC(OC(C)OC(OCC)=O)=O)=O
Synonyms

Debio-0827
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

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (300 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Thibault K, et al. Antinociceptive and anti-allodynic effects of oral PL37, a complete inhibitor of enkephalin-catabolizing enzymes, in a rat model of peripheral neuropathic pain induced by vincristine. European journal of pharmacology. 2008 Dec 14;600(1-3):71-7. [Content Brief]

[2]. Menéndez L, et al. Inhibition of osteosarcoma-induced thermal hyperalgesia in mice by the orally active dual enkephalinase inhibitor PL37. Potentiation by gabapentin. European journal of pharmacology. 2008 Oct 31;596(1-3):50-5. [Content Brief]

[3]. Tesfaye S, et al. PL37: a new hope in the treatment of painful diabetic neuropathy?. Pain management. 2016 Apr;6(2):129-32. [Content Brief]

[4]. Descheemaeker A, et al. Dual enkephalinase inhibitor PL37 as a potential novel treatment of migraine: evidence from a rat model. Brain : a journal of neurology. 2022 Aug 27;145(8):2664-2670. [Content Brief]

[5]. Rossignol J, et al. Synergistic effect of combining dual enkephalinase inhibitor PL37 and sumatriptan in a preclinical model of migraine. Headache. 2024 Mar;64(3):243-252. [Content Brief]

[6]. Ashina M. Targeting enkephalins and pituitary adenylate cyclase-activating polypeptide (PACAP) in migraine. Brain. 2022 Aug 27;145(8):2619-2620. [Content Brief]

[7]. Poras H, et al. Protection of endogenous enkephalins by PL37, a dual NEP/APN inhibitor induces potent analgesic responses p.o. in neuropathic pain [poster]. XXth International Symposium on Medicinal Chemistry (EFMC-ISMC 2008); 2008 Aug 31–Sep 4; Vienna, Austria.

[8]. González-Rodríguez S, et al. Involvement of enkephalins in the inhibition of osteosarcoma-induced thermal hyperalgesia evoked by the blockade of peripheral P2X3 receptors. Neuroscience letters. 2009 Nov 20;465(3):285-9. [Content Brief]

[9]. Zhang M, et al. Discovery of a mitochondria-targeted propranolol conjugate PL37 that induces mitophagy for potent anti-hemangioma activity. Bioorganic & medicinal chemistry. 2026 Oct;141:118750. [Content Brief]

[10]. Mei HR, et al. Efficacy of dual enkephalinase inhibition in a preclinical migraine model is mediated by activation of peripheral delta opioid receptors. Headache. 2023 May;63(5):621-633. [Content Brief]

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PL37

All Opioid Receptor Isoforms

All Aminopeptidase Isoforms

All MMP Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

PL37 Related Classifications

HY-19876 Related Classifications

Bioz