top of page

7 things to know about buprenorphine

Updated: Jan 26, 2020

Buprenorphine is a familar partial mu agonist opioid that is useful for acute pain management in veterinary patients. But it has an interesting pharmacologic profile that produces some surprising clinical results.


1) Subcutaneous administration is unreliable

Subcutaneous administration of 0.02 mg/kg buprenorphine does not result in predictable clinical effect. Choose the IV or IM route!

When working with the traditional concentration of injectable buprenorphine (0.3 mg/mL), the most reliable and effective route of administration is IV, followed by IM and oral transmucosal (OTM) administration. In one study, absorption of buprenorphine from the subcutaneous space of cats was so erratic that pharmacokinetic modeling could not be performed. (1) Clinically, the subcutaneous route of buprenorphine administration does not appear to provide adequate analgesia following OVH in cats (2).


2) Oral transmucosal administration can be used in cats - and dogs, but you may want to increase the dose.

The OTM (sometimes referred to as "buccal") route of administration is in fairly routine use in cats but it can be employed for dogs as well. Bioavailability of 0.02 mg/kg OTM buprenorphine in dogs was about 40%, whereas 0.12 mg/kg (yup, 120 mcg/kg) was almost 50% in one study (3); both doses provided analgesia that was not significantly different from IV administration, though the study was underpowered (4). The volume and expense of buprenorphine at 0.12 mg/kg becomes prohibitive in anything but the smallest dogs and though I do occasionally prescribe OTM buprenorphine in dogs for outpatient analgesia, I typically start with a lower dose (maybe 0.04 - 0.05 mg/kg) and then try to gauge the animal's response, increasing if needed.


3) Alternate formulations exist, including a high concentration version and a sustained release version.

Simbadol is a concentrated (1.8 mg/mL) buprenorphine approved for subcutaneous use in cats. In the suggested dose range (0.12 - 0.24 mg/kg), you can expect to achieve adequate plasma concentrations with subcutaneous administration (unlike lower doses - see #1). Simbadol can also be administered via the oral transmucosal route but the length of action appears to be signifcantly shorter than 24 hours. Of note, Simbadol is currently the least expensive version of buprenorphine available (on a per mg basis) and it can be administered IV to dogs and cats at typical doses (~0.02 - 0.04 mg/kg) to reduce costs associated with buprenorphine analgesia.

A compounded sustained release (SR) version of buprenorphine exists and can provide analgesia for up to 3 days after injection. The matrix is a water-insoluble compound that precipitates in bodily fluids and then slowly releases buprenorphine. Plenty of anecdotal evidence and various studies indicate it can be used in a variety of species but there are a few things to be cautious about:

1) Compounded drugs should be prescribed for an individual patient, according to FDA rules.

2) Inflammatory reactions have been reported at the site of injection in cats.

3) Doses used in dogs should be half that of cats to avoid lethargy and inappetance.


4) Buprenorphine can reverse opioid-induced hyperthermia in cats - but it can also cause it.


I do not get too worried about post-anesthetic hyperthermia in cats unless the patient gives me a behavioral reason to intervene (panting, excessive activity, etc) or a pretty darn elevated body temperature is documented, like around 105 F or higher. If I do feel the need to try to bring down a cat's body temperature that I believe is related to full mu agonist opioid administration (such as hydromorphone) but I still want to keep some analgesia on board, one option is to administer buprenorphine (butorphanol or ultra low dose naloxone can also work). But all opioids, including buprenorphine, have been implicated in post-anesthetic elevations in feline body temperature. It is uncommon that a patient has such a serious temperature elevation associated with buprenorphine administration that intervention is necessary, but in that case, I give some naloxone and repeat as necessary. If the patient still requires analgesia, consider NSAIDs, ketamine, or dexmedetomidine.


5) Buprenorphine has a relatively slow onset and long duration due to sluggish receptor kinetics and hysteresis between plasma concentration & effect.

For me, this is one of the reasons why I do not often utilize it in the preanesthetic time period. Part of my preventive analgesic strategy is to administer a pre-emptive analgesic and, logistically, it can be hard to get buprenorphine working well prior to nociceptive input. I expect some clinical effect within 20 minutes but it may take as long as an hour to have a maximal effect.


The other reason I don't use buprenorphine much as a premedicant is because it is usually not very sedating.


6) Buprenorphine's potency is many times that of morphine - but that does not mean it is always a good at producing analgesia

This just has to do with the difference between efficacy - that is, actual clinical effect - and potency - which basically refers to molecular affinity and activity at the receptor. The literature indicates that buprenorphine is 25 - 100x as potent as morphine, depending on the pain model used. This means that to a certain extent, you can use a many times lower dose to get the same clinical effect. However, due to buprenorphine's inability to completely activate the mu opioid receptor, there is a ceiling effect on it's ability to provide analgesia. What this means for me clinically is simply that buprenorphine may not always be adequate for severely painful conditions and sometimes you just need to employ a full mu agonist opioid. The best way to know is to pain score your patients and titrate analgesia to effect.


7) Buprenorphine may result in additive or antagonist results when mixed with other classes of opioids.

Buprenorphine is partial mu agonist and a kappa antagonist. So what happens if you co-administer it with a full mu agonist like fentanyl? The clinical effect when mixing classes of opioids could be additive if the full mu agonist concentration is low but it might actually reverse the full mu agonist if its concentration is high. This is just another situation in which you have to pain score your patient. Take a careful look at your patient when mixing classes of opioids and make sure that what you think should be happening clinically is actually happening!


1) Vet Anaesth Analg. 2013 Jan;40(1):83-95. Pharmacokinetic and pharmacodynamic modelling of intravenous, intramuscular and subcutaneous buprenorphine in conscious cats. Steagall PV, Pelican L, Giordano T, Auberge C, Sear JW, Luna SP, Taylor PM.


2) Vet Anaesth Analg. 2010 Jul;37(4):357-66. Postoperative analgesic effects of intravenous, intramuscular, subcutaneous or oral transmucosal buprenorphine administered to cats undergoing ovariohysterectomy.


3) Giordano T, Steagall PV, Ferreira TH, Minto BW, de Sá Lorena SE, Brandan J, Luna SP.

Vet Ther. 2008 Summer;9(2):83-93. Pharmacokinetics of buprenorphine following intravenous and oral transmucosal administration in dogs. Abbo LA, Ko JC, Maxwell LK, Galinsky RE, Moody DE, Johnson BM, Fang WB.


4) J Am Vet Med Assoc. 2011 Feb 1;238(3):318-28. Efficacy of oral transmucosal and intravenous administration of buprenorphine before surgery for postoperative analgesia in dogs undergoing ovariohysterectomy.

Ko JC, Freeman LJ, Barletta M, Weil AB, Payton ME, Johnson BM, Inoue T.

57,400 views3 comments

Recent Posts

See All
bottom of page